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Showing results for tags 'bacteria'.
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More Than Half of Human Gut Bacteria Could Be Harmed by Glyphosate
Scott Adams posted an article in Latest Research
Celiac.com 12/07/2020 - A team of researchers has established the first bioinformatics method to determine and test the potential biological sensitivity of living organisms to glyphosate, the chemical in the herbicide commercially marketed as Roundup. Their research shows that glyphosate may negatively affect more than half of bacteria strains that make up the human gut microbiome. The research team included Lyydia Leinoa,Tuomas Talla, Marjo Helandera, Irma Saloniemia, Kari Saikkonen, Suvi Ruuskanena, and Pere Puigbòacd. They are variously affiliated with the Department of Biology, University of Turku, Turku, Finland, the Biodiversity Unit, University of Turku, Finland, the Nutrition and Health Unit, Eurecat Technology Centre of Catalonia, Reus, Catalonia, Spain, and the Department of Biochemistry and Biotechnology, Rovira i Virgili University, Tarragona, Catalonia, Spain. The team managed to identify the enzyme targeted by the broad-spectrum herbicide, glyphosate, and offers the first bioinformatics method for determining potential glyphosate sensitivity. Glyphosate targets an enzyme called 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) in the shikimate pathway, which synthesizes three essential aromatic amino acids (phenylalanine, tyrosine and tryptophan) in plants. "Based on the structure of the EPSPS enzyme, we are able to classify 80-90% of microbial species into sensitive or resistant to glyphosate," says Docent Pere Puigbò, developer of the new bioinformatics tool. Glyphosate has been regarded as safe to use because shikimate pathway is found only in plants, fungi and bacteria. However, the widespread use of glyphosate may reduce the diversity and composition of microbial communities, including the human gut microbiome. The team's new method has allowed them to create a dataset of EPSPS sequences from thousands of species that will enable major research advances. The method resulted in the classification of sequences from nearly 90% of eukaryotes and more than 80% of prokaryotes. Analysis made with the team's new bioinformatics tool shows that more than half of the human core gut bacterial species are potentially sensitive to glyphosate. "This groundbreaking study provides tools for further studies to determine the actual impact of glyphosate on human and animal gut microbiota and thus to their health," explains Docent Marjo Helander. Read more at the Journal of Hazardous Materials -
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Celiac.com 08/27/2020 - Several thousand strains of bacteria live in the human gut. Some strains are beneficial, while others can promote disease. To make matters more difficult, many of these strains cannot currently be grown in laboratory settings. Certain bacteria species that cannot live in oxygen-rich environments present an even more difficult study challenge. A team of biological and mechanical engineers at MIT have created a device for growing oxygen-intolerant bacteria in tissue in low-oxygen conditions that mirror the lining of the human colon, allowing them to live for up to four days. The research team used the device to grow a strain of bacteria called Faecalibacterium prausnitzii, which lives in the human gut and protects against inflammation. They also showed that these bacteria, which are often diminished in patients with Crohn's disease, appear to exert many of their protective effects through the release of a fatty acid called butyrate. The research team included senior authors Linda Griffith, a School of Engineering Professor of Teaching Innovation in MIT's Department of Biological Engineering, and MIT mechanical engineering professor David Trumper, together with lead authors, Jianbo Zhang and Yu-Ja Huang, both postdoctoral students. The researchers also plan to use their system to study various bacteria linked to Crohn's disease, to assess the effects of each species of the condition. The team plans to joins forces with Alessio Fasano, division chief of pediatric gastroenterology and nutrition at Massachusetts General Hospital, to study mucosal tissue from people with celiac disease, and other GI conditions. Tissues grown using this method could help to reveal the secrets of microbe-induced inflammation in cells with differing genetic composition. "We are hoping to get new data that will show how the microbes and the inflammation work with the genetic background of the host, to see if there could be people who have a genetic susceptibility to having microbes interfere with the mucosal barrier a little more than other people," Griffith says. Griffith says the device can be used to study other types of mucosal barriers, including those of the female reproductive tract, such as the cervix and the endometrium. Better understanding the composition of gut bacteria, and their roles in gut inflammation and other celiac-related conditions could pave the way for major breakthroughs in the understanding and treatment of celiac disease. Read more at News-medical.net -
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The Plagues of Pandora’s Box on Humankind
John B. Symes, D.V.M. posted an article in Spring 2010 Issue
Celiac.com 09/21/2019 (Originally published 04/05/2010) - I am a veterinarian who is doing research on the origins of disease. This came about after my miraculous recovery from multiple ailments following my diagnosis of food intolerance, particularly celiac disease. I have chronicled my recovery and findings on my website, www.dogtorj.com. I’ve come to the conclusion that most of what we call “diseases” are long-term symptoms arising from the “civil war” taking place in our bodies, between its residents—our cells and those entities designed to help and protect those residents (e.g. viruses and bacteria) and the constant barrage of immune challenges that we throw at them (e.g. food lectins, carcinogens, chemicals/preservatives, trans fats, fluoride (an “antibiotic” and carcinogen) air pollution, etc., etc. These, coupled with our horrific fast-food diets, inadequate sleep/exercise/sunlight, and self-induced misery through alcohol/drug abuse and our penchant for sugar have brought all of the plagues of Pandora’s Box on humankind. Yet we keep pointing the finger at microorganisms like viruses and bacteria, including L-forms and mollicutes, as the enemy. Granted, most don’t know or fully understand the true nature of viruses and bacteria - that they are crucial for our survival, being important instruments in our adaptation to this ever-changing environment in which we live. But shouldn’t intelligent people be asking why these guys are so ubiquitous yet a relative few people are suffering from the “diseases” caused by these “culprits? The fact is that viruses and L forms do what they do because they need to survive because they are crucial to our survival. Would you disagree that if we could snap our fingers and make all viruses and bacteria disappear from the planet that the entire ecosystem would collapse? Certainly, we know that the vast majority of these bacteria are not pathogenic? What really distinguishes a pathogen from a saprophyte—or a helper? When huge numbers of the population are infected with various “pathogenic” bacteria and yet remain asymptomatic, shouldn’t it give us pause? Why do they become such culprits of disease in the “unfortunate” few? Are they just unfortunate or have they done something—or lived somewhere, in the case of pollution—that has brought this plague on themselves? We know that the number one risk of developing legionnaire’s disease was/is cigarette smoking. Now there’s a surprise. I believe down to my core that viruses and bacteria work in concert to help us all, especially when it comes to adaptation and survival. Bacteria form L-forms and viruses mutate because they need to survive - they are critical to our survival and only become pathogens when we have forced them into doing so with the laundry list of abuses given above. Cancer is little more than a virus (and/or an intracellular bacteria) forcing that cell to duplicate out of control in a desperate attempt to protect itself, and the cell it was designed to protect, as well as escaping those noxious elements (we call them “carcinogens”) that have forced them into this final phase of adaptation. Our immune systems tried valiantly to deal with this during the preceding “autoimmune” phase, a term I no longer use because the thought of our immune system attacking itself for no reason is preposterous, especially in light of research on L-forms. And, we can’t say we weren’t warned by the broad array of symptoms we were given: the heartburn; IBS; allergies; hives; cough; migraines; seizures; fatigue/depression; etc.; etc. Certainly, there are those who have become so afflicted and immune challenged that they need some pharmaceutical aid to deal with these helper-turned-“culprit” bacteria but to become dependent upon antibiotics for any significant length of time is both potentially dangerous and unnecessary. If we stop the assault we are visiting on these misunderstood and reactionary residents, we can come off the drugs (like I did) and re-establish the status quo, and long before the two or three year mark in most cases, I believe. People simply need to know that we are the culprit, not these microorganisms at which we keep pointing our scientific fingers. Why? Because these organisms—the viruses, bacteria, L-forms and mollicutes—are here to stay! It is we who are the transient visitors. And if we want to enjoy our stay, we’re going to have to learn how to treat ourselves, and those who reside within us, a whole lot better. -
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Celiac.com 12/26/2018 - The first wave of results are in from the 2015 FDA-mandated post-market surveillance studies of duodenoscopes, and they are not encouraging. The duodenoscopes are designed to be reprocessed, to be cleaned and disinfected, according to manufacturer guidelines. However, reprocessed scopes show "higher-than-expected" rates of contamination with dangerous bacteria. In a recent safety announcement, the FDA revealed that 3% of properly collected samples tested positive for more than 100 colony-forming units of "low-concern" organisms. These bacteria are not likely to cause serious infections, but they do indicate "reprocessing failure." Moreover, an additional 3% of properly collected samples tested positive for "high-concern" bacteria that are more often associated with disease, such as Escherichia coli or Staphylococcus aureus. In 2013, the FDA began to focus on a possible connection between multi‒drug resistant bacteria and reprocessed duodenoscopes. In 2015, FDA ordered duodenoscope makers Olympus, Fujifilm, and Pentax to determine whether healthcare facilities were able to properly clean and disinfect the devices. The mandatory monitoring is part of the FDA’s effort to eliminate patient infections associated with bacteria from contaminated duodenoscopes. The FDA’s order required the companies to conduct two separate studies. First, they were required to sample and culture reprocessed duodenoscopes to learn more about issues that contribute to contamination. Second, they were required to evaluate the training of hospital staff in following the reprocessing instructions as part of a study of “human factors.” When the companies failed to carry out such studies promptly, The FDA sent warning letters citing their failure publicly. All three device makers have now begun collecting the required data. They recently completed testing for the initial human factors, and at least 10% of the samples have been collected for the sampling and culturing study. Initial findings from the human factors study of staff training indicate that staff finds the reprocessing instructions in current user manuals difficult to comprehend and follow, the FDA said. The FDA is working with the duodenoscope manufacturing companies to revise and clarify the user materials to improve reprocessing outcomes and to reduce contamination risk. Source: medscape.com -
Celiac.com 11/13/2018 - Ubiquitin is highly conserved across eukaryotes and is essential for normal eukaryotic cell function. The bacterium Bacteroides fragilis is part of the standard human gut microbiome, and the only bacterium known to encode a homologue of eukaryotic ubiquitin. The B. fragilis gene sequence points to a previous horizontal gene transfer from a eukaryotic source. The sequence encodes a protein (BfUbb) with 63% identity to human ubiquitin, which is exported from the bacterial cell. Is molecular mimicry of human ubiquitin by gut microbe linked to autoimmune diseases like celiac disease? A team of researchers recently set out to determine if there was antigenic cross‐reactivity between B. fragilis ubiquitin and human ubiquitin and also to determine if humans produced antibodies to BfUbb. The research team included L. Stewart, J. D. M. Edgar, G. Blakely and S. Patrick. They are variously affiliated with the School of Biological Sciences, University of Edinburgh, Edinburgh, UK; the School School of Biological Sciences, Queen’s University Belfast, Belfast, UK; the Regional Immunology Laboratory, Belfast Health and Social Care Trust, Belfast, UK; and the Wellcome‐Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast, UK. Molecular model comparisons of BfUbb and human ubiquitin predicted likely structural similarity with 99.8% confidence. The team used linear epitope mapping to identify cross-reacting epitopes in BfUbb and human ubiquitin. Also, at least one epitope of BfUbb does not cross‐react with human ubiquitin. The team used enzyme‐linked immunosorbent assay to compare the reaction of human serum to BfUbb and human ubiquitin from 474 subjects among four groups: (1) newly autoantibody‐positive patients, (2) allergen‐specific immunoglobulin (Ig)E‐negative patients, (3) ulcerative colitis patients and (4) healthy volunteers. The team’s data show that the exposure to BfUbb into the human immune system triggers the creation of IgG antibodies. Patients referred for first‐time autoimmune disease testing are more likely to have a high levels of antibodies to BfUbb than are healthy volunteer subjects. From this, the team concludes that molecular mimicry of human ubiquitin by BfUbb could be a trigger for autoimmune disease. Finding and understanding potential triggers for autoimmune conditions helps to take us one step further to understanding and potentially curing celiac disease. Stay tuned for further developments in their arena. First published: 04 August 2018 https://onlinelibrary.wiley.com/doi/full/10.1111/cei.13195 -
Can Targeting Gut Bacteria Prevent Autoimmune Disease?
Jefferson Adams posted an article in Latest Research
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. -
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 -
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. -
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.
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Could Changing Gut Bacteria Prevent Celiac Disease?
Jefferson Adams posted an article in Latest Research
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. -
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.
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Gut Bacteria Play Significant Role in Gluten Metabolism
Jefferson Adams posted an article in Latest Research
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 -
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 -
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.
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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
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Can Bacteria Help Researchers Better Diagnose Celiac Disease?
Jefferson Adams posted an article in Latest Research
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 -
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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 -
How Celiac Disease Alters Intestinal Bacteria in Adults
Gryphon Myers posted an article in Latest Research
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 -
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 -
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 -
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. -
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
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