• Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Announcements

    • Scott Adams

      Frequently Asked Questions About Celiac Disease   04/24/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What is Celiac Disease and the Gluten-Free Diet? What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes

Search the Community

Showing results for tags 'bacteria'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Forums

  • Celiac Disease: Diagnosis, Recovery, Related Disorders & Research
    • Gluten-Free and Celiac Disease Calendar of Events
    • Celiac Disease - Pre-Diagnosis, Testing & Symptoms
    • Celiac Disease - Post Diagnosis, Recovery/Treatment(s)
    • Celiac Disease - Related Disorders & Research
    • Dermatitis Herpetiformis
    • Gluten Intolerance and Behavior
  • Celiac Disease Support & Help
    • Celiac Disease - Coping With
    • Celiac Disease - Parents of Kids or Babies With Celiac Disease
    • Gab/Chat Room - To Discuss Anything BUT Celiac Disease / Gluten-Free Diet
    • Celiac Disease - Doctors
    • Celiac Disease - Teenagers & Young Adults Only
    • Celiac Disease - Pregnancy
    • Celiac Disease - Friends and Loved Ones of Celiacs
    • Celiac Meeting Room
    • Celiac Disease - Sleep
    • Celiac Disease - Support Groups
  • Gluten-Free Lifestyle
    • Gluten-Free Foods, Products, Shopping & Medications
    • Gluten-Free Recipes - Baking & Cooking Tips
    • Gluten-Free Restaurants
    • Gluten-Free Ingredients & Food Labeling Issues
    • Celiac Disease - Publications & Publicity
    • Gluten-Free Travel
    • Gluten-Free Diet & Weight Issues
    • Gluten-Free International Room (Outside USA)
    • Gluten-Free Sports and Fitness
  • When A Gluten-Free Diet Just Isn't Enough
    • Other Food Intolerance and Leaky Gut Issues
    • Super Sensitive Celiacs & Gluten Sensitive
    • Alternative Diets
  • Forum Technical Assistance
    • Board/Forum Technical Help
  • DFW/Central Texas Celiacs's Events
  • DFW/Central Texas Celiacs's Groups/Organizations in the DFW area

Calendars

  • Gluten-Free Community Calendar

Blogs

There are no results to display.

There are no results to display.

Categories

  • Celiac.com Sponsors
  • Celiac Disease
  • Safe Gluten-Free Food List / Unsafe Foods & Ingredients
  • Gluten-Free Food Reviews
  • Gluten-Free Recipes
    • Gluten-Free Recipes: American & International Foods
    • Gluten-Free Recipes: Biscuits, Rolls & Buns
    • Gluten-Free Recipes: Noodles & Dumplings
    • Gluten-Free Dessert Recipes: Pastries, Cakes, Cookies, etc.
    • Gluten-Free Bread Recipes
    • Gluten-Free Flour Mixes
    • Gluten-Free Kids Recipes
    • Gluten-Free Recipes: Snacks & Appetizers
    • Gluten-Free Muffin Recipes
    • Gluten-Free Pancake Recipes
    • Gluten-Free Pizza Recipes
    • Gluten-Free Recipes: Soups, Sauces, Dressings & Chowders
    • Gluten-Free Recipes: Cooking Tips
    • Gluten-Free Scone Recipes
    • Gluten-Free Waffle Recipes
  • Celiac Disease Diagnosis, Testing & Treatment
  • Miscellaneous Information on Celiac Disease
    • Additional Celiac Disease Concerns
    • Celiac Disease Research Projects, Fundraising, Epidemiology, Etc.
    • Conferences, Publicity, Pregnancy, Church, Bread Machines, Distillation & Beer
    • Gluten-Free Diet, Celiac Disease & Codex Alimentarius Wheat Starch
    • Gluten-Free Food Ingredient Labeling Regulations
    • Celiac.com Podcast Edition
  • Celiac Disease & Gluten Intolerance Research
  • Celiac Disease & Related Diseases and Disorders
    • Lists of Diseases and Disorders Associated with Celiac Disease
    • Addison's Disease and Celiac Disease
    • Anemia and Celiac Disease
    • Anorexia Nervosa, Bulimia and Celiac Disease
    • Arthritis and Celiac Disease
    • Asthma and Celiac Disease
    • Ataxia, Nerve Disease, Neuropathy, Brain Damage and Celiac Disease
    • Attention Deficit Disorder and Celiac Disease
    • Autism and Celiac Disease
    • Bacterial Overgrowth and Celiac Disease
    • Cancer, Lymphoma and Celiac Disease
    • Candida Albicans and Celiac Disease
    • Canker Sores (Aphthous Stomatitis) & Celiac Disease
    • Casein / Cows Milk Intolerance and Celiac Disease
    • Chronic Fatigue Syndrome and Celiac Disease
    • Cognitive Impairment and Celiac Disease
    • Crohn's Disease and Celiac Disease
    • Depression and Celiac Disease
    • Dermatitis Herpetiformis: Skin Condition Associated with Celiac Disease
    • Diabetes and Celiac Disease
    • Down Syndrome and Celiac Disease
    • Dyspepsia, Acid Reflux and Celiac Disease
    • Epilepsy and Celiac Disease
    • Eye Problems, Cataract and Celiac Disease
    • Fertility, Pregnancy, Miscarriage and Celiac Disease
    • Fibromyalgia and Celiac Disease
    • Flatulence (Gas) and Celiac Disease
    • Gall Bladder Disease and Celiac Disease
    • Gastrointestinal Bleeding and Celiac Disease
    • Geographic Tongue (Glossitis) and Celiac Disease
    • Growth Hormone Deficiency and Celiac Disease
    • Heart Failure and Celiac Disease
    • Infertility, Impotency and Celiac Disease
    • Inflammatory Bowel Disease and Celiac Disease
    • Intestinal Permeability and Celiac Disease
    • Irritable Bowel Syndrome and Celiac Disease
    • Kidney Disease and Celiac Disease
    • Liver Disease and Celiac Disease
    • Lupus and Celiac Disease
    • Malnutrition, Body Mass Index and Celiac Disease
    • Migraine Headaches and Celiac Disease
    • Multiple Sclerosis and Celiac Disease
    • Myasthenia Gravis Celiac Disease
    • Obesity, Overweight & Celiac Disease
    • Osteoporosis, Osteomalacia, Bone Density and Celiac Disease
    • Psoriasis and Celiac Disease
    • Refractory Celiac Disease & Collagenous Sprue
    • Sarcoidosis and Celiac Disease
    • Scleroderma and Celiac Disease
    • Schizophrenia / Mental Problems and Celiac Disease
    • Sepsis and Celiac Disease
    • Sjogrens Syndrome and Celiac Disease
    • Skin Problems and Celiac Disease
    • Sleep Disorders and Celiac Disease
    • Thrombocytopenic Purpura and Celiac Disease
    • Thyroid & Pancreatic Disorders and Celiac Disease
    • Tuberculosis and Celiac Disease
  • The Origins of Celiac Disease
  • Gluten-Free Grains and Flours
  • Oats and Celiac Disease: Are They Gluten-Free?
  • Frequently Asked Questions
  • Journal of Gluten Sensitivity
    • Journal of Gluten Sensitivity Spring 2018 Issue
    • Journal of Gluten Sensitivity Winter 2018 Issue
    • Journal of Gluten Sensitivity Autumn 2017 Issue
    • Journal of Gluten Sensitivity Summer 2017 Issue
    • Journal of Gluten Sensitivity Spring 2017 Issue
    • Journal of Gluten Sensitivity Winter 2017 Issue
    • Journal of Gluten Sensitivity Autumn 2016 Issue
    • Journal of Gluten Sensitivity Summer 2016 Issue
    • Journal of Gluten Sensitivity Spring 2016 Issue
    • Journal of Gluten Sensitivity Winter 2016 Issue
    • Journal of Gluten Sensitivity Autumn 2015 Issue
    • Journal of Gluten Sensitivity Summer 2015 Issue
    • Journal of Gluten Sensitivity Spring 2015 Issue
    • Journal of Gluten Sensitivity Winter 2015 Issue
    • Journal of Gluten Sensitivity Autumn 2014 Issue
    • Journal of Gluten Sensitivity Summer 2014 Issue
    • Journal of Gluten Sensitivity Spring 2014 Issue
    • Journal of Gluten Sensitivity Winter 2014 Issue
    • Journal of Gluten Sensitivity Autumn 2013 Issue
    • Journal of Gluten Sensitivity Summer 2013 Issue
    • Journal of Gluten Sensitivity Spring 2013 Issue
    • Journal of Gluten Sensitivity Winter 2013 Issue
    • Journal of Gluten Sensitivity Autumn 2012 Issue
    • Journal of Gluten Sensitivity Summer 2012 Issue
    • Journal of Gluten Sensitivity Spring 2012 Issue
    • Journal of Gluten Sensitivity Winter 2012 Issue
  • Celiac Disease Support Groups
    • United States of America: Celiac Disease Support Groups and Organizations
    • Outside the USA: Celiac Disease Support Groups and Contacts
  • Celiac Disease Doctor Listing
  • Kids and Celiac Disease
  • Gluten-Free Travel
  • Gluten-Free Cooking
  • Gluten-Free
  • Allergy vs. Intolerance
  • Tax Deductions for Gluten-Free Food
  • Gluten-Free Newsletters & Magazines
  • Gluten-Free & Celiac Disease Links
  • History of Celiac.com
    • History of Celiac.com Updates Through October 2007
    • Your E-mail in Support of Celiac.com 1996 to 2006

Found 27 results

  1. Celiac.com 04/25/2018 - A team of Yale University researchers discovered that bacteria in the small intestine can travel to other organs and trigger an autoimmune response. In this case, they looked at Enterococcus gallinarum, which can travel beyond the gut to the spleen, lymph nodes, and liver. The research could be helpful for treating type 1 diabetes, lupus, and celiac disease. In autoimmune diseases, such as type 1 diabetes, lupus, and celiac disease, the body’s immune system mistakenly attacks healthy cells and tissues. Autoimmune disease affects nearly 24 million people in the United States. In their study, a team of Yale University researchers discovered that bacteria in the small intestine can travel to other organs and trigger an autoimmune response. In this case, they looked at Enterococcus gallinarum, which can travel beyond the gut to the spleen, lymph nodes, and liver. They found that E. gallinarum triggered an autoimmune response in the mice when it traveled beyond the gut. They also found that the response can be countered by using antibiotics or vaccines to suppress the autoimmune reaction and prevent the bacterium from growing. The researchers were able to duplicate this mechanism using cultured human liver cells, and they also found the bacteria E. gallinarum in the livers of people with autoimmune disease. The team found that administering an antibiotic or vaccine to target E. gallinarum suppressed the autoimmune reaction in the mice and prevented the bacterium from growing. "When we blocked the pathway leading to inflammation," says senior study author Martin Kriegel, "we could reverse the effect of this bug on autoimmunity." Team research team plans to further investigate the biological mechanisms that are associated with E. gallinarum, along with the potential implications for systemic lupus and autoimmune liver disease. This study indicates that gut bacteria may be the key to treating chronic autoimmune conditions such as systemic lupus and autoimmune liver disease. Numerous autoimmune conditions have been linked to gut bacteria. Read the full study in Science.
  2. Celiac.com 08/30/2017 - The human gut is home to a huge and diverse number of microorganisms that perform various biological roles. Disturbances in a healthy gut microbiome might help to trigger various inflammatory diseases, such as multiple sclerosis (MS). Human gut-derived commensal bacteria suppress CNS inflammatory and demyelinating disease. Can they improve the treatment of multiple Sclerosis (MS)? A team of researchers recently set out to evaluate evidence that gut commensals may be used to regulate a systemic immune response and may, therefore, have a possible role in treatment strategies for multiple Sclerosis. The research team included Ashutosh Mangalam, Shailesh K. Shahi, David Luckey, Melissa Karau, Eric Marietta, Ningling Luo, Rok Seon Choung, Josephine Ju, Ramakrishna Sompallae, Katherine Gibson-Corley, Robin Patel, Moses Rodriguez, Chella David, Veena Taneja, and Joseph Murray. In a recent article, the team reports on their identification of human gut-derived commensal bacteria, Prevotella histicola, which can suppress experimental autoimmune encephalomyelitis (EAE) in a human leukocyte antigen (HLA) class II transgenic mouse model. P. histicola suppresses disease through the modulation of systemic immune reactions. P. histicola challenge caused a reduction in pro-inflammatory Th1 and Th17 cells and an increase in CD4+FoxP3+ regulatory T cells, tolerogenic dendritic cells, and suppressive macrophages. This study indicates that gut commensals may regulate a systemic immune response, and so may have a role in future treatments for multiple Sclerosis, and possibly other autoimmune diseases such as celiac disease. Source: Cell.com. DOI: http://dx.doi.org/10.1016/j.celrep.2017.07.031
  3. Celiac.com 10/21/2016 - Researchers at Boston University's Henry M. Golden School of Dental Medicine have identified a metabolic enzyme that alerts the body to invading bacteria, which may lead to new treatments for celiac disease. A research team that set out to isolate and identify the enzymes and evaluate their potential as novel enzyme therapeutics for celiac disease, reports that the enzymes exhibit exceptionally high gluten-degrading enzyme activities, and are "naturally associated with bacteria that colonize the oral cavity." Rothia bacteria, found in human saliva, can break down gluten compounds that cause an exaggerated immune response and that are typically resistant to the digestive enzymes that mammals produce. The team was able to isolate a new class of gluten-degrading enzymes from Rothia mucilaginosa, an oral microbial colonizer. The Rothia enzymes in question belong to the same class as food-grade Bacillus enzymes. The researchers noted that "B. subtilis is food safe and has been consumed for decades, e.g. in a product called natto, a Japanese fermented soy bean dish." B. subtilis and its products have been safely consumed by humans for many hundreds of years, with very few problems reported. They add that the "…food-grade status of B. subtilis, and the already widely consumed natto products, open new avenues for potential therapeutic applications of the subtilisin enzymes." The Rothia subtilisins and two subtilisins from Bacillus licheniformis, subtilisin A and the food-grade Nattokinase, efficiently degraded the immunogenic gliadin-derived 33-mer peptide and the immunodominant epitopes recognized by the R5 and G12 antibodies. This study identified as promising new candidates for enzyme therapeutics in celiac disease. Based on these results, the research team concludes that gluten-degrading Rothia and food-grade Bacillus subtilisins are the "preferred therapy of choice for celiac disease," and that their exceptional enzymatic activity, along with their connection to natural human microbial colonizers, make them "worthy of further exploration for clinical applications in celiac disease and potentially other gluten-intolerance disorders." Their study appears in the American Journal of Physiology—Gastrointestinal and Liver Physiology.
  4. Celiac.com 08/01/2016 - Symptoms and damage in celiac disease is caused by partially-degraded gluten peptides from wheat, barley and rye. Susceptibility genes are necessary to trigger celiac disease, but they can't do it alone. Some researchers suspect that these susceptibility genes might get help from conditions resulting from unfavorable changes in the microbiota. To better understand the whole picture, a team of researchers recently set out to examine gluten metabolism by opportunistic pathogens and commensal duodenal bacteria, and to characterize the ability of the resulting peptides to activate gluten-specific T-cells from celiac patients. The research team included A Caminero, HJ Galipeau, JL McCarville, CW Johnston, S Bernier, AK Russell, J Jury, AR Herran, J Casqueiro, JA Tye-Din, MG Surette, NA Magarvey, D Schuppan, and EF Verdu. They are variously affiliated with the Farncombe Family Digestive Health Research Institute, and the Department of Biochemistry & Biomedical Sciences, M. G. DeGroote Institute for Infectious Disease Research at McMaster University, Hamilton, Ontario, Canada; the Immunology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, Australia; the Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia; Área de Microbiología, Facultad de Biología y Ciencias Ambientales, Universidad de León, León, 24071 Spain; the Immunology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, 3052 Australia; the Department of Gastroenterology, The Royal Melbourne Hospital, Grattan St., Parkville, Victoria, 3050 Australia, and the Institute for Translational Immunology and Research Center for Immunotherapy, University Medical Center, Johannes Gutenberg University, Mainz, Germany. For their study, the team colonized germ-free C57BL/6 mice with bacteria isolated from the small intestine of celiac patients or healthy controls, selected by their in vitro gluten-degrading capacity. They then measured gliadin levels and proteolytic action in intestinal contents after gluten feeding. Using peripheral blood mononuclear cells from celiac patients after receiving a 3-day gluten challenge, the research team characterized by LC-MS/MS the eptides produced by bacteria used in mouse colonizations from the immunogenic 33-mer gluten peptide. They found that the bacterial colonizations created clear gluten degradation patterns in the small intestine of the mice. Pseudomonas aeruginosa (Psa), an opportunistic pathogen from celiac patients, exhibited elastase activity and produced peptides that better translocated the mouse intestinal barrier. Psa-modified gluten peptides activated gluten-specific T-cells from celiac patients. In contrast, Lactobacillus spp. from the duodenum of non-celiac controls degraded gluten peptides produced by human and Psa proteases, reducing their immunogenicity. From these data, the research team concludes that small intestinal bacteria show clear gluten metabolic patterns in vivo, increasing or reducing gluten peptide immunogenicity. This microbe-gluten-host interaction may modulate autoimmune risk in genetically susceptible persons and may underlie any connection between celiac disease and microbial imbalance or maladaptation in the digestive tract. Source: Gastroenterology. 2016 Jun 30. pii: S0016-5085(16)34713-8. doi: 10.1053/j.gastro.2016.06.041.
  5. Celiac.com 11/20/2015 - A Canadian researcher has discovered what might be a big step toward preventing celiac disease. Dr. Elena Verdú, an associate professor at the Farncombe Family Digestive Health Research Institute at McMaster University, has found that bacteria in the gut may contribute to the body's response to gluten. If her discovery pans out, it may be possible to treat, or even prevent, celiac disease by changing the the type of bacteria in the gut. "By changing the type of bacteria in the gut, we could change the inflammatory response to gluten," says Verdú. So far, researchers have been unable to explain why 30 per cent of people have genes that can cause celiac disease, but only 2 to 5 per cent actually develop it. Also a mystery is why the disease develops at any age. Higher rates of celiac disease are being driven not just be better testing and awareness, but also by external triggers. According to Dr. Decker Butzner, a Calgary-based pediatric gastroenterologist, there are another triggering factor which we've never understood…[t]here is an environmental trigger." Researchers have known for some time that people with celiac disease have different types of gut bacteria than those without celiac disease, but they didn't whether the changes in gut bacteria were caused by celiac disease, or the other way around. Verdú's study, which found that the inflammatory response to gluten was impacted by gut microbiota, is the first study to show that it is the gut microbes are likely triggering celiac disease. The study appears in the American Journal of Pathology. Read more at TheSpec.com.
  6. Celiac.com 02/09/2015 - Do you suffer from persistent celiac symptoms in spite of following a strict gluten-free diet and having normal small bowel mucosa? Many celiac patients do. Moreover, typical explanations, such as accidental gluten-intake or the presence of other gastrointestinal disease, do not account for all of the symptoms in these patients. Recent studies have suggested that changes in intestinal microbiota are associated with autoimmune disorders, including celiac disease. A team of researchers recently set out to determine if abnormal intestinal microbiota may in fact be associated with persistent gastrointestinal symptoms in gluten-free celiac disease patients. The research team included Pirjo Wacklin PhD, Pilvi Laurikka, Katri Lindfors PhD, Pekka Collin MD, Teea Salmi MD, Marja-Leena Lähdeaho MD, Päivi Saavalainen PhD, Markku Mäki MD, Jaana Mättö PhD, Kalle Kurppa MD, and Katri Kaukinen MD. They are variously associated with the Finnish Red Cross Blood Service, Helsinki, Finland; School of Medicine, University of Tampere, Tampere, Finland; the Tampere Centre for Child Health Research at the University of Tampere and Tampere University Hospital in Tampere, Finland; the Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, in Tampere, Finland; the Department of Dermatology at Tampere University Hospital in Tampere, Finland; the Research Programs Unit of the Immunobiology, and Department of Medical Genetics at the Haartman Institute of the University of Helsinki in Helsinki, Finland; the Department of Internal Medicine at Tampere University Hospital in Tampere, and with Seinäjoki Central Hospital in Seinäjoki, Finland, The team used 16S rRNA gene pyrosequencing to analyze duodenal microbiota in 18 gluten-free celiac patients suffering from persistent symptoms, and 18 gluten-free celiac patients without symptoms. All celiac patients had been following a strict gluten-free diet for several years, and had restored small bowel mucosa and tested negative for celiac autoantibodies. The team rated symptoms using the Gastrointestinal Symptom Rating Scale, and found that gluten-free celiac disease patients with persistent symptoms had different duodenal bacteria than celiac patients without symptoms. Gluten-free celiac patients with persistent symptoms had a higher relative abundance of Proteobacteria (P=0.04) and a lower abundance of Bacteroidetes (P=0.01) and Firmicutes (P=0.05). Moreover, they had a much narrower range of bacteria types in their guts. The discovery that dysbiosis of microbiota is associated with persistent gastrointestinal symptoms in gluten-free celiac patients offers a new avenue of treatment for such patients. Source: Am J Gastroenterol. 2014;109(12):1933-1941.
  7. Celiac.com 08/06/2014 - Although the role of human digestive proteases in gluten proteins is quite well known, researchers don’t know much about the role of gut bacteria in the metabolism of these proteins. A research team recently set out to explore the diversity of the cultivable human gut microbiome involved in gluten metabolism. Their goal was to isolate and characterize human gut bacteria involved in the metabolism of gluten proteins. The team included Alberto Caminero, Alexandra R. Herrán, Esther Nistal, Jenifer Pérez-Andrés, Luis Vaquero, Santiago Vivas, José María G. Ruiz de Morales, Silvia M. Albillos and Javier Casqueiro. They are variously associated with the Instituto de Biología Molecular, Genómica y Proteómica (INBIOMIC), the Área de Microbiología, Facultad de Biología y Ciencias Ambientales, and the Instituto de Biomedicina (IBIOMED) Campus de Vegazana at the Universidad de León, León, Spain, and with the Departamento de Gastroenterología, Hospital de León, the Departamento de Inmunología y, Hospital de León, and with Instituto de Biotecnología (INBIOTEC) de León all in León, Spain. For their study, they cultured twenty-two human fecal samples, with gluten as the principal nitrogen source. They also isolated 144 strains from 35 bacterial species potentially involved in gluten metabolism in the human gut. They found 94 strains that metabolise gluten, while 61 strains showed an extracellular proteolytic activity against gluten proteins. In patients with celiac disease, several strains exhibited peptidasic activity towards the 33-mer peptide, an immune-triggering peptide. Most of the gluten-metabolizing strains belong to the phyla Firmicutes and Actinobacteria, mainly from the genera Lactobacillus, Streptococcus, Staphylococcus, Clostridium and Bifidobacterium. Their findings show that the human intestine hosts numerous bacteria that can use gluten proteins and peptides for food. These bacteria could have an important role in gluten metabolism and could give rise to new treatments for celiac disease. Source: FEMS Microbiology Ecology, Volume 88, Issue 2, pages 309–319, May 2014. DOI: 10.1111/1574-6941.12295
  8. Celiac.com 03/24/2014 - Two new studies have confirmed colonization of gluten-degrading bacteria in the human mouth and in the upper gastrointestinal tracts respectively. Both studies come out of the Department of Periodontology and Oral Biology, Boston University Henry M. Goldman School of Dental Medicine in Boston, Massachusetts. The research teams included Maram Zamakhchari, Guoxian Wei, Floyd Dewhirst, Jaeseop Lee, Detlef Schuppan, Frank G. Oppenheim, and Eva J. Helmerhorst. Gluten is notoriously hard for mammals to digest, because gliadin proteins resist mammalian proteolytic enzymes in the gut, so researchers wanted to find sources of gluten-digesting microbial enzymes from the upper gastro-intestinal tract. These microbial enzymes have the potential to neutralize the gluten peptides that act as celiac disease triggers. In the first study the researchers assessed proteolytic activity in suspended dental plaque towards a) gliadin-derived paranitroanilide(pNA)-linked synthetic enzyme substrates a mixture of natural gliadins and c) synthetic highly immunogenic gliadin peptides (33-mer of α2-gliadin and 26-mer of γ-gliadin). In addition, they conducted gliadin zymography to establish the approximate molecular weights and pH activity profiles of the gliadin-degrading oral enzymes and performed liquid iso-electric focusing to determine overall enzyme iso-electric points. Their results provide the first known evidence of gluten-degrading microorganisms associated with the upper gastro-intestinal tract. Such microorganisms may play a hitherto unappreciated role in the digestion of dietary gluten and thus protection from celiac disease in subjects at risk. In the second study, the team employed a selective plating strategy using gluten agar to obtain oral microorganisms with gluten-degrading capacity. They then used16S rDNA gene sequencing to carry out microbial speciations. To determine enzyme activity, they used gliadin-derived enzymatic substrates, gliadins in solution, gliadin zymography, and 33-mer a-gliadin and 26-mer c-gliadin immunogenic peptides. They separated fragments of the gliadin peptides by RP-HPLC, and structurally characterized them using mass spectrometry. They found that strains Rothia mucilaginosa and Rothia aeria showed high gluten-degrading activity. For example, gliadins (250 mg/ml) added to Rothia cell suspensions (OD620 1.2) degraded by 50% after 30 minutes of incubation. Importantly, the 33-mer and 26-mer immunogenic peptides were also cleaved, primarily C-terminal to Xaa-Pro-Gln (XPQ) and Xaa-Pro-Tyr (XPY). The major gliadin-degrading enzymes produced by the Rothia strains were 70–75 kDa in size, and the enzyme expressed by Rothia aeria was active over a wide pH range (pH 3–10). While the human digestive enzyme system lacks the capacity to cleave immunogenic gluten, such activities are naturally present in the oral microbial enzyme repertoire. Taken together, these studies suggest a potential for these bacteria to fuel the development of compounds that can degrade of harmful gluten peptides that trigger celiac disease in susceptible individuals. Source: PLoS One. 2011;6(9):e24455. doi: 10.1371/journal.pone.0024455. http://www.ncbi.nlm.nih.gov/pubmed/20948997
  9. Hello everyone, I just want to share my story and see if it sounds like I have DH. I was never diagnosed by a dermatologist, this was a self-diagnosis, but I have many reasons to believe that I am right. I am a 25 year old caucasian female. I consumed gluten for most of my life until the age of 21 or so; then, I developed a weird lesion on my neck that would not go away. I tried different antibiotics, but nothing worked. Then, more lesions started popping up on my neck and then face. Sometimes they would form a line pattern, so I suspected sporotrichosis and took some antifungals, which helped at first, but then stopped helping. The lesions were huge, like the size of a dime, but they mostly hurt and leaked pus (sorry this is gross); however they did not look like boils (that I see on some DH pictures); I think they immediately came out as open sores, but of course I might have picked at them without realizing at the time (being on adderal did not improve things). Their center would be pretty hard and moist, and filled with what looked like granules of some sort. They never really itched (still do not itch); however, they do hurt/sting, rubbing them feels sorta good so I guess they do kinda itch (I am confused lol), but the one on my lip REALLY stings, if I start picking at it, tears would start flowing from my eyes involuntarily. It feels like a thousand pins in my lip. Also, after healing, they would leave a purple and white scar that would not go away and stand out against the rest of the skin; the ones on my face are actually idented sorta like cystic acne scars; the one on my nose is uneven and bumpy. Sometimes the scars would form a mini-blister that would be painful and unproductive to pop; sometimes they would form a pimple. I (mostly) do not eat gluten anymore except rare random exposure due to my forgetfulness or lack of food to eat (the other day I bought Rafaellos and ate a couple before realizing they do have some gluten in them; but I take Gluten Cutter, not sure if that works or not). So, anyways, to summarize: - The lesions do not exactly itch, but they definitely sting/burn, and it feels good to rub some of them (not my lip, that is too painful). - If I remember correctly, they never looked like blisters, and started with pretty large open sores. - If I get an outbreak now, it will start looking almost exactly like a pimple, but if I try to squeeze it, it is a painful, hard, watery blister with nothing coming out. It feels like there is a cluster of granules under the blister. Sometimes it starts as a brown, VERY TOUGH piece of tissue (a little crust that is almost impossible to rip off, later it falls off by itself and a regular crust forms). - The lesions leave scars that are either indented or discolored or both. Even the scars still feel kinda prickly and they never go away. - Cutting down on my gluten intake decreased the number and severity of outbreaks, but I still do get them from time to time. Right now my face does not look so good without make-up. The weirdest part: At some point I though I had Morgellons disease, and my lesions did look exactly like the Morgellons lesions with little "roots", etc; I was also finding fibers on my skin and even under my skin. I am not sure if I was losing my mind or what, but I even studied samples of my skin under microscope and found ingrown fibers, etc. Later those symptoms mysteriously vanished when I started cutting down on gluten intake. I am still not sure what it was. So can anyone relate to this? I am REALLY interested in your feedback! Thanks!
  10. The article describes mice with leaky gut like condition and behavior issues that are improved by a bacteria. From Scientific American site: http://www.scientificamerican.com/article.cfm?id=bacterium-reverses-autism-like-behavior-in-mice ... Doses of a human gut microbe helped to reverse behavioral problems in mice with autism-like symptoms, researchers report today in Cell. The treatment also reduced gastrointestinal problems in the animals that were similar to those that often accompany autism in humans. ... The autistic mice also had 'leaky guts', in which the walls of the intestine break down and allow substances to leak through. Several studies have found that humans with autism are also more likely to have gastrointestinal disorders, suggesting that the two problems may be linked. ...
  11. Celiac.com 05/02/2013 - Even though gluten-free baked goods are getting slowly better than in the past, many gluten-free baked goods on the market today taste worse than their traditional counterparts made with wheat flour, and may also lead to nutritional deficiencies of vitamins, minerals and fiber. Thus, the production of high-quality gluten-free products has become a very important issue. Microbial fermentation using lactic acid bacteria and yeast is one of the most ecological sensitive and economically sound methods of producing and preserving food. A team of researchers recently set out to determine how microbial fermentation with lactic acid bacteria might be used to make better gluten-free products. The research team included E. Zannini, E. Pontonio, D.M. Waters, and E.K.Arendt of the School of Food and Nutritional Sciences at the University College Cork in Western Road, in Cork, Ireland. Their recent article in Applied Microbiology and Microtechnology reviews the role of sourdough fermentation in creating better quality gluten-free baked goods, and for developing a new concept of gluten-free products with therapeutic and health-promoting characteristics. Source: Appl Microbiol Biotechnol. 2012 Jan;93(2):473-85. doi: 10.1007/s00253-011-3707-3.
  12. Celiac.com 02/22/2013 - Scientists estimate that about 1% of the global population has celiac disease. For those who suffer, following a gluten-free diet is the only treatment available. Among doctors such treatment is known as 'medical nutritional therapy (MNT).' Recently, researchers have paid more attention to sourdough lactic acid bacteria as a way to improve the therapeutic benefits of gluten-free bread and baked goods for people on a gluten-free diet due to celiac disease. A team of researchers recently set out to assess use of sourdough lactic acid bacteria as a cell factory for delivering functional biomolecules and food ingredients in gluten free bread. The research team included Elke K Arendt, Alice Moroni and Emanuele Zannini. They are variously affiliated with the School of Food and Nutritional Sciences at University College Cork, Western Road, and the National Food Biotechnology Centre at University College Cork, in Cork, Ireland. More and more, consumers are demanding higher quality gluten-free bread, clean labels and natural products. Still, replacing gluten in bread presents significant technological challenges due to the low baking performance of gluten free products (gluten-free). Sourdough has been used since ancient times to improve quality, nutritional properties and shelf life of traditional breads, sourdough fermentation may offer a better solution for commercial production of gluten-free breads. In a recent issue of Microbial Cell Factories, the research team highlights how sourdough lactic acid bacteria can be an efficient cell factory for delivering functional biomolecules and food ingredients to enhance the quality of gluten free bread. Source: Microbial Cell Factories 2011, 10(Suppl 1):S15. doi:10.1186/1475-2859-10-S1-S15
  13. Celiac.com 01/30/2013 - Currently, doctors diagnose celiac disease with blood tests that screen for two antibodies, one that targets gluten and another that goes after an intestinal protein. The tests work pretty well to spot advanced cases of celiac disease, but by that time, patients are already suffering intestinal damage. A research team looking into a method for reliable earlier detection of celiac disease focused on the responses of certain bacteria to celiac disease. They have built a library of peptides on the surfaces of bacteria which capture new antibodies associated with celiac disease. This, in turn, has led them to a new technique for harvesting celiac disease antibodies, which may help improve diagnosis for celiac disease, especially early on. The researchers say the technique may allow them to successfully tell, much earlier than before, which perspective celiac sufferers are sick and which are healthy. The research team included Bradley N. Spatola, Joseph A. Murray, Martin Kagnoff, Katri Kaukinen, and Patrick S. Daugherty. They are affiliated with the Department of Chemical Engineering at the University of California at Santa Barbara, California, the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, the Laboratory of Mucosal Immunology, Department of Medicine and the Department of Pediatrics at the University of California at San Diego in La Jolla, California and with the Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland. For their study, Patrick Daugherty, of the University of California, Santa Barbara, and his team aimed to find previously unknown disease-linked antibodies. Their strategy centered on building an enormous library of random peptide sequences to find ones that would bind to the antibodies. To create their library, the researchers inserted one billion random peptide genes into Escherichia coli, with one peptide gene per bacterium. Once the genes were expressed inside the bacteria, thousands of copies of the peptides migrated to the cells’ surface. The researchers hoped that some of these peptides would bind antibodies from the blood of people with early-stage celiac disease, but not those in samples from healthy people. The team hoped that their approach, with numerous bacteria each bearing a different peptide, would be more likely to identify unknown antibodies than are current types of peptide libraries, which must be mounted on hard surfaces. To test their new library approach, the researchers collected blood samples from 40 healthy people and 45 people who had been diagnosed with celiac disease. They purified antibodies from the blood samples, then labeled antibodies from half the celiac patients with a green fluorescent dye and the rest of the patients’ antibodies with a red dye. They then mixed the peptide-coated bacteria together with all the antibodies, adding five times as many unlabeled antibodies from the healthy subjects to block labeled antibodies from binding to peptides found in people with and without celiac disease. Next, they sorted the cells, collecting only those bacteria displaying both red and green fluorescence. Cells labeled with both dyes, the researchers reasoned, help a peptide that could bind to an antibody found in at least two people, one patient from each group. These antibodies, they say, could be markers for celiac disease. Additional screening of the peptides with antibodies from healthy patients and those with celiac disease, the researchers narrowed the bacterial pool down to six unique peptides, none of which bind to known celiac antibodies. The researchers then measured binding between these peptides and the full suite of antibodies from patients’ blood. Based on that data, they used a statistical analysis to conclude that they could identify correctly 85% of people with celiac disease and 91% of healthy – nearly matching the values of existing diagnostic tests. It remains uncertain whether this approach will permit doctors to diagnose celiac disease at earlier stages than current methods, but the results look promising, and the team remains hopeful. Daugherty says that the method is applicable to other immune disorders, including difficult-to-diagnose illnesses such as lupus, multiple sclerosis, and some cancers. Source: Anal. Chem., 2013, 85 (2), pp 1215–1222. DOI: 10.1021/ac303201d
  14. Celiac.com 05/30/2012 - From what we understand about celiac disease, both genetic and environmental factors play a part in its development: eople with certain genetic dispositions are more likely to develop it, but studies of twins at high risk of developing celiac disease have shown that in 25% of cases, only one of the twins will develop the disease. This indicates an environmental effect, and with more research it might be possible to discover what these environmental factors are so that parents with celiac disease can take steps to prevent their children from developing the disease themselves. Breast-feeding has already demonstrated some protective effect on infants at risk of developing celiac disease, but it is still unclear how the modulation of intestinal bacteria affects the formation of the disease. Understanding the role various strains of intestinal bacteria play in the intestine could be the key to understanding why breast-feeding helps prevent celiac disease, and perhaps why celiac disease develops at all. In the present study, 75 newborns with at least one first degree relative with celiac disease were broken into breast-feeding, formula-feeding groups, high (7-28%) and low (less than 1%) genetic risk groups, then tested at 7 days, 1 month and 4 months for prevalence and diversity of intestinal bacteria. Infants at high risk of developing celiac disease had more Bacteroides vulgatus, regardless of feeding methods while infants at low risk of developing celiac disease had more Bacteroides ovatus, Bacteroides plebeius and Bacteroides uniformis. Formula-fed infants had more Bacteroides intestinalis, Bacteroides caccae and Bacteroides plebeius, though prevalence depended on the testing stage. The most striking finding of the experiment seems to indicate that both low genetic risk of celiac disease development and breast-feeding are positively correlated with the prevalence of Bacteroides uniformis in the intestines. This might explain why breast-feeding can help protect against development of the disease, by introducing more Bacteroides uniformis into the infant's intestinal bacteria community. The implications of this research are still unclear, but a follow-up study on these infants is intended. Further research may explain how the prevalence of these bacteria in the intestine actually affects the development of celiac disease in infants. Source: http://www.ncbi.nlm.nih.gov/pubmed/21642397
  15. Celiac.com 05/23/2012 - We know from past studies that the intestinal bacteria communities of children with celiac disease differ greatly from those of healthy children, but there has been little work done to draw such a correlation with adult celiac disease sufferers. Intestinal bacteria could potentially serve as a convenient way of indexing the severity of a patient's celiac disease, but research in adults is limited. A recent study remedies this, showing that adults with celiac disease do, in fact, have different intestinal bacteria from healthy adults, which may lead to a way of testing for the severity of one's disorder based on fecal bacteria tests. Ten untreated celiac disease patients, eleven treated celiac disease patients (those on gluten-free diets for at least two years) and eleven healthy adults were tested for intestinal bacteria in fecal samples. The healthy adults were tested once under normal gluten diet conditions, and additionally, ten of them were tested again after one week of gluten-free dieting. Testing showed that untreated celiac disease patients had much more Bifidobacterium bifidum in their intestinal microbial communities than those of healthy adults. Treated celiac disease patients showed decreased levels of Bifidobacterium bifidum, as well as a reduction in the diversity of Lactobacillus and Bifidobacterium. These results most closely resembled those achieved by healthy adults. It would seem, then, that a gluten-free diet helps to balance and normalize intestinal bacteria populations. While a portion of the treated celiac disease patients displayed restored, normal intestinal bacteria, there were still differences in the presence of short-chain fatty acids. Such SCFAs would appear to correlate with celiac disease, regardless of the diet taken: healthy adults, both on gluten-free diets and on normal diets had significantly fewer SCFAs than both treated and untreated celiac disease patients. Gluten-free, healthy adults had the fewest, but treated celiac disease patients actually had the highest. We can take from this study that gluten-free diets help to lower both the presence and diversity of bacteria associated with celiac disease. A gluten-free diet does not 'fix' the presence of short-chain fatty acids in the intestines though, even though it is not entirely clear what these acids signal as to the health of the individual. Source: http://www.ncbi.nlm.nih.gov/pubmed/22542995
  16. Celiac.com 10/13/2011 - While certain immunologic risk factors have been identified for celiac disease, it is still unclear why some develop the disease and others do not. One possibility is that some people are more able to digest gluten than others. Those who cannot break down the gluten into smaller proteins higher in the digestive tract, in the mouth and stomach, could develop an immune reaction to the full, unaltered protein. Maram Zamakhchari and other researchers at Boston University and collaborating sites investigated whether bacteria present in the mouth can play a role in breaking down gluten. The authors reported in the journal PLoS ONE, published by the Public Library of Science, that two bacterial species present in the normal oral flora were able to degrade gluten. The species are Rothia mucilaginosa and Rothia aeria, as the authors reported in the online version of the publication on September 21, 2011. This finding raises the question of whether people with celiac disease have different levels of these bacteria than those without celiac disease. The species R. mucilaginosa is found in the mouth and the intestines while R. aeria is only found in the mouth. The authors attempted to answer this question by looking at saved intestinal biopsy specimens from patients with and without celiac disease. They found no difference in the presence of the intestinal bacteria between celiacs and healthy patients. This study supports the idea that bacteria in the digestive tract may play a role in the development of celiac disease. While there was no difference in gluten-digesting bacteria in the intestines of celiac patients, the study did not evaluate the bacteria levels in the mouth. Patients with celiac disease have an increased incidence of Sjogren's syndrome, which features decreased mouth saliva, and suggests that oral digestion could be related to developing celiac disease. Assessing the presence of these bacteria in the mouths of celiacs versus the general population will be an important next step in the research. Source: Identification of Rothia Bacteria as Gluten-Degrading Natural Colonizers of the Upper Gastro-Intestinal Tract. PLoS ONE 6(9): e24455. doi:10.1371/journal.pone.0024455
  17. Celiac.com 03/15/2011 - For celiacs, it's not really the cinnamon bun that's the enemy. Nor the pizza crust, nor the ravioli. It's the gliadin in these foods - the alcohol-soluble portion of the gluten protein - that's the real culprit. Gliadin is the "gladiator" of the human digestive tract. When we ingest gliadin, enzymes try to break it down into a form that can be absorbed by the small intestine. But gliadin resists, fighting hard to remain intact. A regular small intestine has, like any good fortress, a protective wall: the mucosal lining of the intestine. This layer of mucus normally acts as a barrier against gliadin's assaults. But in a celiac intestine, the mucosal lining is permeable. With gliadin's destructive power enhanced by its enzyme sidekick, tissue Transglutaminase (tTG), it quickly gets past this poorly-guarded layer. Scientists are working to put their finger on exactly what makes the mucosal lining of a celiac's small intestine so permeable. Now a January study by Czech researchers found at least one thing that affects the permeability of the intestinal mucosa: gut bacteria. In this study, called "Role of Intestinal Bacteria in Gliadin-Induced Changes in Intestinal Mucosa: Study in Germ-Free Rats", researchers tied off sections of rats' intestines and introduced various kinds of bacteria to each section. They wanted to measure the effect that these bacteria had on the intestinal mucus - or more specifically, on the goblet cells that produce the intestinal mucus. To ensure that the kinds of bacteria in the rats' intestines were under experimental control, the rats had been raised from birth in germ-free conditions. They found that introducing gliadin to the intestines had the effect of decreasing the mucus-producing cells, thereby eroding the intestines' protective layer. No big surprises there - gliadin is a fighter, a digestive "gladiator", after all. But when they added strains of so-called harmful bacteria, Escherichia coli (otherwise known as E coli) or Shigella, the mucus-producing cells decreased even more. The cells first secreted massive amounts of mucus, then promptly exhausted themselves and gave up. This left the intestine looking very similar to that of a person in the early stages of celiac disease, say the researchers. But the tale did indeed have a happy ending. Along came the good bacteria, Bifidobacterium bifidum (or "Biff" for short). The mucus-producing cells in the small intestine increased when Biff was present. In fact, Biff was able to partially reverse the mucus-decreasing effects of E coli and Shigella. The researchers concluded that the composition of gut bacteria has an effect on the protective mucus of the intestines: an overgrowth of bad bacteria decreases the protective layer, while the addition of good bacteria increases the protective layer. Their study may eventually lead to treatment options for human celiacs, by finding ways to protect tender intestines from the harmful effects of gliadin. Source: PLoS One. 2011 Jan 13;6(1):e16169
  18. Celiac,com 10/08/2010 - Many people are familiar with probiotics, such as acidophilus, Bifidobacterium bifidum, Bifidobacterium longum, Lactobacillus acidophilus, Lactobacillus case, which promote beneficial gut bacteria, and are commonly found in yogurt, kefir and other fermented milk products. But how many of us have heard of polysaccharides, which are a particular kind of carbohydrate made up of of a number of monosaccharides joined together by something called glycosidic bonds. On a simpler note, polysaccharides are also known as pre-biotics, because they serve as fuel for probiotic bacteria, and help to promote healthy ratios of beneficial bacteria to non-beneficial bacteria in the gut. It is well-known among scientists that diet has a major influence on the health and diversity of gut microbiota. People with celiac disease must follow a gluten-free diet in order to avoid associated damage and health disorders. When people with celiac disease follow a gluten-free diet, their celiac symptoms disappear and their gut begins to heal itself from the damage. The health effects of the diet for people with celiac disease are overwhelmingly positive. However, there is some evidence that by eliminating gluten, people with celiac disease are making themselves susceptible to a plunge in beneficial gut bacteria, and an elevated ratio of bad-to-good gut bacteria. This may have immune-system implications for those people. To test this hypothesis, a team of scientists recently conducted a preliminary study to determine if a gluten-free diet alone could change the make-up and immune properties of gut microbiota. The team included G. De Palma, I. Nadal, M. C. Collado, and Y. Sanz. Their full results appear in theSeptember, 2009 issue of the British Journal of Nutrition. To briefly summarize their study, the team enrolled ten healthy individuals without celiac disease, averaging just over 30 years of age. They put these people on a gluten-free diet for a month. Subsequent analysis of fecal microbiota and dietary intake showed a decrease in healthy gut bacteria, coupled with an increase of unhealthy bacteria that corresponded with reduced intake of polysaccharides after following the gluten-free diet. Another healthy control group that ate a diet that contained gluten, and thus provided polysaccharides. In addition representing an adversely change in gut microbiota, the samples taken while the individuals followed a gluten-free diet also exerted reduced immune stimulatory effects on peripheral blood mononuclear cells than those of subjects on a regular gluten-containing, polysaccharide-rich diet. Should these findings be confirmed by subsequent studies, the results could call attention to a more comprehensive approach to proper dietary intake in people with celiac disease, including dietary counseling, and possible supplementation of the diet with polysaccharides. Source: Br J Nutr. 2009 Oct;102(8):1154-60.
  19. Celiac.com 03/19/2010 - Celiac disease is a chronic inflammatory disorder of the gut triggered by an adverse immune response to dietary gluten proteins in genetically susceptible individuals. One of the first ways the body responds to offending proteins in an adverse celiac disease response is by producing mucous via IgA secretion in an effort to neutralize offending antigens and pathogens. A team of researchers recently sought to better document the relationships between immunoglobulin-coated bacteria and bacterial composition in feces of celiac disease patients, untreated and treated with a gluten-free diet (GFD) and healthy controls. The research team included Giada De Palma, Inmaculada Nadal, Marcela Medina, Ester Donat, Carmen Ribes-Koninckx, Miguel Calabuig, and Yolanda Sanz. They observed that intestinal dysbiosis and reduced immunoglobulin-coated bacteria are associated with celiac disease in children. Both untreated and treated celiac disease patients showed markedly lower levels of IgA, IgG and IgM-coated fecal bacteria compared to healthy controls. Celiac disease patients showed substantially reduced ratio of Gram-positive to Gram-negative bacteria compared to control subjects. Untreated celiac disease patients showed less abundant group proportions (P<0.050) of Bifidobacterium, Clostridium histolyticum, C. lituseburense and Faecalibacterium prausnitzii than did healthy controls. Untreated celiac disease patients showed more abundant group proportions (P<0.050) of Bacteroides-Prevotella than in control subjects. Both untreated and treated celiac disease patients showed significantly impoverished (P<0.050) levels of IgA coating the Bacteroides-Prevotella compared with healthy controls. From these results, the research team concluded that intestinal dysbiosis plays a role in reduced IgA-coating bacteria in celiac disease patients. This offers a fresh perspective into the possible relationships between the gut microbiota and the host defenses in celiac disease patients. Source: BMC Microbiology 2010, 24 February
  20. Research indicates that rod-shaped bacteria, of the species Clostridium, Prevotella, and Actinomyces, in the proximal small intestine may contribute to some cases of celiac disease in children. Recent data builds on previous research by the team from 1985 to 1996, which proved that rod-shaped bacteria were present in the proximal small intestine of Swedish children with celiac disease, but not in those without celiac disease. For the current study, Sten Hammarström and colleagues from Umeå University in Sweden used an electron microscope to scan proximal small intestine biopsies from 45 children with celiac disease taken between 2004 and 2007, and 18 without the condition. To identify the bacteria, they used 16S ribosomal DNA sequencing in DNA extracted from biopsies washed with solution containing an agent that enriches bacteria attached to the epithelial lining. In healthy children with no celiac disease, Streptococcus and Neisseria bacteria are most common of the normal, mucosa-associated microbial flora of the proximal small intestine, along with a limited number of other genera, including Veillonella, Gemella, Actinomyces, Rothia, and Hemophilus. Surprisingly, the researchers found that microbial flora of the proximal small intestine in biopsies from celiac disease patients differed only slightly from that of the control subjects. Only a single biopsy tested positive for rod-shaped bacteria. This finding made the team to look more closely at the microbial flora of nine frozen celiac disease samples that showed the presence of rod-shaped bacteria. In these samples, microbial flora were substantially richer in Clostridium, Prevotella, and Actinomyces compared with biopsies lacking rod-shaped bacteria. The researchers also note that all three types of bacteria could be found in two current celiac disease biopsies taken from children born during the celiac disease epidemic in Sweden in 1985–1996, when the earlier study was carried out. During this time, rates of celiac disease in children younger than 2 years of age increased four-fold. “We hypothesize that the increased frequency of rod-shaped bacteria in the jejuna mucosa of celiac disease children at least partly was due to the changes in infant-feeding practice during that time,” write the researchers. The changes resulted from new national feeding recommendations for infants to delay the introduction of gluten-containing foods from 4 to 6 months. This meant that many more children consumed their first gluten without the protective benefits of breastfeeding, the researchers write. The recommendation was later reversed. The study by Hammarström and co-workers supports their conclusion that these rod-shaped bacteria may contribute to celiac disease in genetically susceptible individuals by uptaking and transforming gluten into large immunogenic peptides, which can then cross with the bacterium through the epithelium, or interfere with the barrier action of the epithelium to permit the passage of gluten into the under-laying tissue. “Such bacteria could be seen as an adjuvant promoting T-cell activation,” they say. “Whether the identified bacteria have any of these properties remain to be elucidated.” Am J Gastroenterol 2009; 104: 3058–3067
  21. Celiac.com 06/09/2009 - Results of a recent small population study done in Spain suggest that a gluten-free diet may change gut bacteria balance by decreasing beneficial bacteria and increasing detrimental bacteria. Certainly, gut health is an issue to most people with celiac disease. Recent studies suggest that people with celiac disease benefit from bifidium and lactobaccilus supplements, so it's possible that such benefit is in part an offsetting of damage due to gluten-free diet; at least, a connection seems possible. The Spanish study follows just ten individuals for just one month on gluten-free diets. A large-scale, long-term study might make very different observations, and reach very different conclusions. The study found no significant differences in dietary intake before and after the gluten-free diet except for reductions (P=0.001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P=0.007, P=0.031 and P=0.009, respectively) as a result of the GFD analysed by fluorescence in situ hybridisation (FISH). Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P=0.020, P=0.001 and P=0.017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P=0.005 and P=0.003) after the GFD assessed by quantitative PCR (qPCR). TNF-alpha, interferon-gamma, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P=0.021, P=0.037, P=0.002 and P=0.007, respectively) after the diet. The study doesn't provide any real evidence to support a conclusion one way or the other, especially their conclusion that a gluten-free diet "may constitute an environmental variable to be considered in treated Coeliac disease patients for its possible effects on gut health." The fact is that beneficial, probiotic bacteria in the human gut are influenced by diet. The more fruits, vegetables, and high fiber foods we consume, the healthier our bacteria will be. The Spanish study makes no mention of the subjects' diets. Were they fed high fiber, low fat diets rich in fruits and vegetables, or did they eat a standard western diet with no gluten? It would be interesting to compare the gut bacteria levels of people before celiac disease diagnosis and after celiac disease diagnosis to see if a gluten-free diet improves gut bacteria overall, or if the Spanish results would be seen again. Br J Nutr. 2009 May 18:1-7.
  22. Celiac.com 03/09/2009 - A team of researchers based in Finland recently demonstrated for the first time that B. lactis probiotic bacteria are capable of shielding epithelial cells from cellular damage caused by gliadin exposure. The research team was made up of doctors K. Lindfors, T. Blomqvist, K. Juuti-Uusitalo, S. Stenman, J. Venäläinen, M. Mäki and K. Kaukinen. They are associated with the Paediatric Research Centre for the Medical School of the Finland’s University of Tampere, the Department of Peadiatrics, and the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital, and the Department of Pharmacology and Toxicology of the Finland’s University of Kuopio. In people with celiac disease, wheat gliadin causes serious intestinal symptoms and damages the small-bowel mucosa. Untreated, this can leave the individual at risk of developing various cancers and numerous associated conditions. Most all of this can be reversed or prevented if detected and treated early enough. Currently, the only effective treatment for celiac disease is a strict life-long gluten-free diet. However, a 100% gluten-free diet is nearly impossible to maintain, with so many gluten-free products containing trace amounts of gluten. Because of this, people with celiac disease face regular gluten contamination. Also because of this, acceptable alternatives are desirable. Earlier studies have indicated that probiotic bacteria might be used in sourdough fermentation to induce the hydrolysis of celiac toxic gluten in food manufacturing, and thereby benefit people with celiac disease. Although several studies have addressed the ability of probiotic bacteria to detoxify gliadin after an extensive incubation period, the team found none that investigated whether various live probiotic bacteria can inhibit gliadin-induced toxic effects directly on epithelial cells. In this study the team set out to determine whether probiotics Lactobacillus fermentum or Bifidobacterium lactis might block the toxic effects of gliadin in intestinal cell culture conditions. To assess the degree to which live probiotics were able to block peptic-tryptic digested gliadin-induced degradation of human colon cells Caco-2, the team measured epithelial permeability by transepithelial resistance, actin cytoskeleton arrangements by the extent of membrane ruffling and expression of tight junctional protein ZO-1. B. lactis inhibited the gliadin-induced increase dose-dependently in epithelial permeability, and, at higher concentrations totally eliminated the gliadin-induced reduction in transepithelial resistance. That is, B. lactis decreased or eliminated the compromise in cell-wall resistance caused by gliadin. This means that B. lactis overcame the mechanism that gives rise to the decreased cell resistance and the increased permeability that occurs during an adverse reaction to wheat gliadin. The B. lactis strain also interfered with the creation of membrane ruffles in Caco-2 cells caused by gliadin exposure. Furthermore, it also shielded the tight junctions of Caco-2 cells from the toxic effects of gliadin, as shown by the way in which ZO-1 is expressed. The researchers concluded that live B. lactis bacteria might achieve partial to full blockage of gliadin toxicity gluten/gliadin-induced damage in the small-intestinal mucosa of people with celiac disease, and that it merits further study concerning its potential as a dietary supplement to guard against any silent damage associated with accidental gluten-contamination in celiac disease. Clinical and Experimental Immunology, 152: 552–558
  23. Celiac.com 11/06/2008 - Previously, the possible link between gut bacteria and celiac disease has been discussed in "Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?"[1] A 5-year European study, DIABIMMUNE, is currently underway focusing on some 7000 children, from birth, investigating the development of intestinal bacterial flora and its influence on the development of the human immune system and autoimmune disease, including celiac disease.[2] Hopefully, this study will provide some much needed answers. Now a Spanish group of scientists has produced further evidence supporting a possible role for gut bacteria in the pathogenesis of celiac disease by investigating whether gut microflora present in the feces of celiac disease patients participates in the pro-inflammatory activity of celiac disease.[3] The makeup of fecal microflora in celiac disease patients differs significantly from that of healthy subjects. To determine whether gut microflora is a participant in the pro-inflammatory milieu of celiac disease, the Spanish research team incubated cultures of peripheral blood mononuclear cells from healthy adults with fecal microflora obtained from 26 active celiac disease children, 18 symptom-free celiac disease children on a gluten-free diet, and 20 healthy children. The scientists additionally investigated possible regulatory roles of Bifidobacterium longum ES1 and B. bifidum ES2 obtained from the feces of healthy individuals, co-incubating the Bifidobacterium with the test subject fecal microflora and the peripheral blood mononuclear cell culture. Fecal micrflora from both active and, notably, treated, symptom-free celiac children caused a significant increase in pro-inflammatory cytokine production and a decrease in anti-inflammatory IL-10 production in the peripheral blood mononuclear cell cultures compared to the fecal microflora from healthy children. However, cultures co-incubated with the Bifidobacterium strains exhibited a suppression of the pro-inflammatory cytokine production and an increase in IL-10 production. IL-10 is a cytokine which promotes immune tolerance. The scientists concluded that the makeup of the gut flora of celiacs may contribute to pro-inflammation in celiac disease, possibly in a synergy with gliadin, and that certain strains of Bifidobacterium appear to suppress and reverse pro-inflammatory effects and offering therapeutic opportunities for the treatment of celiac disease. It would have been interesting if the scientists had also investigated the effect of adding vitamin D to the fecal microflora and the peripheral blood mononuclear cell cultures. It is likely the addition of vitamin D might also have resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production. This is borne out by experiments with Mycobacterium tuberculosis and its culture filtrate antigen in peripheral blood mononuclear cell cultures where the addition of vitamin D resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production.[4] It is possible that celiac disease may be entirely prevented in infancy by routinely administrating prophylactic doses of vitamin D and probiotics containing specific strains of Bifidobacterium before gluten is introduced into the infant's diet. The vitamin D and Bifidobacterium strains may provide an IL-10 anti-inflammatory environment in which the immune system learns to respond tolerantly to gluten, forever preventing the onset of celiac disease. The fact that certain strains of fecal Bifidobacterium from healthy individuals appear to suppress celiac disease inflammation brings to mind the concept of "fecal bacteriotherapy" or "fecal transplant", a therapy developed and used in practice by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., known best for his development of a triple-antibiotic treatment for H. pylori and ulcerative colitis.[5] Fecal bacteriotherapy involves transplanting feces from a healthly, screened donor into an ailing patient with a persistant bacterial gastrointestinal disorder whose own gut flora has first been reduced or eliminated with antibiotics. The fecal microflora from the healthy donor reseeds the gut of the ailing patient with a healthy mix of intestinal microflora curing the gastrointestinal disorder. The Bifidobacterium research done by the Spanish researchers suggests that fecal bacteriotherapy might be an option to treat or cure celiac disease in adults, replacing gut flora causing intolerance to gluten with a healthy mix of gut flora that encourages tolerance to gluten. Sources [1] Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease? Roy S. Jamron https://www.celiac.com/articles/21605/ [2] European Study Will Focus On Relation Of Gut Bacteria to Autoimmune Disease in Children Roy S. Jamron https://www.celiac.com/articles/21607/ [3] Journal of Inflammation 2008, 5:19. Bifidobacterium strains suppress in vitro the pro-inflammatory milieu triggered by the large intestinal microbiota of coeliac patients. Medina M, De Palma G, Ribes-Koninckx C, Calabuig M, Sanza Y. http://www.journal-inflammation.com/content/pdf/1476-9255-5-19.pdf [4] J Clin Immunol. 2008 Jul;28(4):306-13. Regulatory role of promoter and 3' UTR variants of vitamin D receptor gene on cytokine response in pulmonary tuberculosis. Selvaraj P, Vidyarani M, Alagarasu K, Prabhu Anand S, Narayanan PR. http://www.springerlink.com/content/d67236620021j84u/ [5] Prof. Thomas J. Borody, M.D., Bio and Publication List http://www.cdd.com.au/html/hospital/clinicalstaff/borody.html http://www.cdd.com.au/html/expertise/publications.html
  24. Celiac.com 06/19/08 - Today in most modern countries, children are being raised in bacteria-free environments, yet studies are seeing a rising incidence of autoimmune disease and allergies. Previous studies have found that Finnish children are six times more likely to have type 1 diabetes and a five times higher rate of celiac disease than Russian children despite equal genetic susceptibility. Over-cleanliness and life-style may be promoting the higher prevalence of these disorders. The Diabimmune study, backed by the EU with EUR 6 million in financing, is asking whether by removing all bacteria, we are not actually weakening our children's immune systems. Led by the University of Helsinki, researchers from 5 European countries will collaborate on Diabimmune, a study involving some 7000 children which will last from 2008-2013. The study will focus on the development of the intestinal bacterial flora after birth, the effect that the living environment has on the composition of the bacterial flora, the effect infections have on the maturation of the human immune system, and the operation of the white blood cells that regulate immune responses. In addition, the researchers will examine whether the protection conferred by infections against autoimmune and allergic responses is associated with the overall infection load or due to specific microbes. It is expected that the results will provide much needed insight into celiac disease, other autoimmune disorders, and allergies. For the first time, researchers will comprehensively monitor the composition of microbes populating the intestines of developing infants and study how the microbes may influence the development of allergies and autoimmune disease, including celiac disease. Finally, conclusive evidence may be found which may answer the question of whether gut bacteria is involved the pathogenesis of celiac disease. Are immune systems becoming lazy? European Research Headlines 18 June 2008 http://ec.europa.eu/research/headlines/news/article_08_06_18_en.html Researchers from five countries to test hygiene hypothesis with EU funding University of Helsinki 29 May 2008 http://www.med.helsinki.fi/english/news/20080529_DIABIMMUNE.htm
  25. This article appeared in the Summer 2008 edition of Celiac.com's Scott-Free Newsletter. Celiac.com 06/16/2008 - Do vitamin D deficiency, gut bacteria, and timing of gluten introduction during infancy all combine to initiate the onset of celiac disease? Two recent papers raise the potential that this indeed may be the case. One paper finds that when transgenic mice expressing the human DQ8 heterodimer (a mouse model of celiac disease) are mucosally immunized with gluten co-administered with Lactobacillus casei bacteria, the mice exhibit an enhanced and increased immune response to gluten compared to the administration of gluten alone.[1] A second paper finds that vitamin D receptors expressed by intestinal epithelial cells are involved in the suppression of bacteria-induced intestinal inflammation in a study which involved use of germ-free mice and knockout mice lacking vitamin D receptors exposed to both friendly and pathogenic strains of gut bacteria.[2] Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not. If one considers these two papers together, one notices: (1) Certain species of gut bacteria may work in conjunction with gluten to cause an increased immune response which initiates celiac disease; (2) The presence of an adequate level of vitamin D may suppress the immune response to those same gut bacteria in such a way as to reduce or eliminate the enhanced immune response to gluten caused by those gut bacteria, thus preventing the onset of celiac disease. Vitamin D has recently been demonstrated to play a role in preserving the intestinal mucosal barrier. A Swedish study found children born in the summer, likely introduced to gluten during winter months with minimal sunlight, have a higher incidence of celiac disease strongly suggesting a relationship to vitamin D deficiency.[3] Recent studies found vitamin D supplementation in infancy and living in world regions with high ultraviolet B irradiance both result in a lower incidence of type 1 diabetes, an autoimmune disease closely linked to celiac disease.[4][5] Gut bacteria have long been suspected as having some role in the pathogenesis of celiac disease. In 2004, a study found rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated children with celiac disease, but not to the epithelium of healthy controls.[6][7] Prior to that, a paper published on Celiac.com[8] first proposed that celiac disease might be initiated by a T cell immune response to "undigested" gluten peptides found inside of pathogenic gut bacteria which have "ingested" short chains of gluten peptides resistant to breakdown. The immune system would have no way of determining that the "ingested" gluten peptides were not a part of the pathogenic bacteria and, thus, gluten would be treated as though it were a pathogenic bacteria. The new paper cited above[1] certainly gives credence to this theory. Celiac disease begins in infancy. Studies consistently find the incidence of celiac disease in children is the same (approximately 1%) as in adults. The incidence does not increase throughout life, meaning, celiac disease starts early in life. Further, in identical twins, one twin may get celiac disease, and the other twin may never experience celiac disease during an entire lifetime. Something other than genetics differs early on in the childhood development of the twins which initiates celiac disease. Differences in vitamin D levels and the makeup of gut bacteria in the twins offers a reasonable explanation as to why one twin gets celiac disease and the other does not. Early childhood illnesses and antibiotics could also affect vitamin D level and gut bacteria makeup. Pregnant and nursing mothers also need to maintain high levels of vitamin D for healthy babies. Sources: [1] Immunol Lett. 2008 May 22. Adjuvant effect of Lactobacillus casei in a mouse model of gluten sensitivity. D'Arienzo R, Maurano F, Luongo D, Mazzarella G, Stefanile R, Troncone R, Auricchio S, Ricca E, David C, Rossi M. http://dx.doi.org/10.1016/j.imlet.2008.04.006 [2] The FASEB Journal. 2008;22:320.10. Meeting Abstracts - April 2008. Bacterial Regulation of Vitamin D Receptor in Intestinal Epithelial Inflammation Jun Sun, Anne P. Liao, Rick Y. Xia, Juan Kong, Yan Chun Li and Balfour Sartor http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/320.10 [3] Vitamin D Preserves the Intestinal Mucosal Barrier Roy S. Jamron https://www.celiac.com/articles/21476/ [4] Arch Dis Child. 2008 Jun;93(6):512-7. Epub 2008 Mar 13. Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis. Zipitis CS, Akobeng AK. http://adc.bmj.com/cgi/content/full/93/6/512 [5] Diabetologia. 2008 Jun 12. [Epub ahead of print] The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide. Mohr SB, Garland CF, Gorham ED, Garland FC. http://www.springerlink.com/content/32jx3635884xt112/ [6] Am J Gastroenterol. 2004 May;99(5):905-6. A role for bacteria in celiac disease? Sollid LM, Gray GM. http://dx.doi.org/10.1111/j.1572-0241.2004.04158.x [7] Am J Gastroenterol. 2004 May;99(5):894-904. Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease. Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML. http://dx.doi.org/10.1111/j.1572-0241.2004.04157.x [8] Are Commensal Bacteria with a Taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease? Roy S. Jamron https://www.celiac.com/articles/779/