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Celiac.com 04/18/2024 - Human gut microbiota contains many viruses, bacteria and fungi. Escherichia coli representatives are facultative anaerobic bacteria in the colon that play a crucial role in the metabolism of lactose, vitamin synthesis and immune system modulation. E. coli forms a biofilm on the epithelial cell surface of the intestine that can be modified by diet compounds, such as gluten, xylitol, lactose and probiotics. Researchers recently examined the impact of probiotic-derived Lactobacillus rhamnosus GG strain on non-pathogenic E. coli biofilm. They also also treated mono- and multi-species biofilm with gluten, xylitol and lactose. The research team included Joanna Kwiecińska-Piróg, Karolina Chomont, Dagmara Fydrych, Stawarz Julita, Tomasz Bogiel, Jana Przekwas, and Eugenia Gospodarek-Komkowska. They arę variously affiliated with the Microbiology Department, Pharmaceutical Faculty, Collegium Medicum in Bydgoszcz, University of Nicolaus Copernicus in Toruń in Bydgoszcz, Poland; and the Clinical Microbiology Division, Antoni Jurasz University Hospital no 1 in Bydgoszcz, Poland. Probiotics May be Helpful in Rebuilding Gut Microbiota After Broad Spectrum Antibiotic Therapy The researchers used 96-well plates to obtain biofilm growth. They stained the biofilm with crystal violet. To evaluate the type of interaction in mono- and multispecies biofilm, a new formula was introduced - biofilm interaction ratio index (BIRI). To describe the impact of nutrients on biofilm formation, they calculated the biofilm formation impact ratio (BFIR). The biofilms formed by both examined species are stronger than in monocultures. All the BIRI values were above 3.0. It was found that the monospecies biofilm of L. rhamnosus is strongly inhibited by gluten (84.5%), while the monospecies biofilm of E. coli is strongly inhibited by xylitol (85.5%). The mixed biofilm is inhibited by lactose (78.8%) and gluten (90.6%). The relations between bacteria in the mixed biofilm led to changes in biofilm formation by E. coli and L. rhamnosus GG. Study Highlights: • Combining E. coli and L. rhamnosus creates a stronger biofilm than when each bacterium is cultured alone. • Adding xylitol to the diet can decrease the formation of biofilms by E. coli bacteria. • Lactose and gluten are less effective than xylitol in reducing the formation of biofilms by E. coli bacteria. The results indicate tha t probiotics might be helpful in rebuilding the gut microbiota after broad spectrum antibiotic therapy, but only if gluten and lactose are excluded from diet. Graphic Abstract Read more at: Sciencedirect.com

Celiac.com 05/29/2023 - Celiac disease is an autoimmune disorder triggered by gluten consumption. While genes and gluten play a significant role in the development of the disease, researchers have started to explore additional factors that contribute to its onset. One intriguing area of study is the gut microbiota, the vast community of microorganisms that reside in our digestive tract. Recent research has suggested that alterations in the gut microbiota may act as an additional risk factor for celiac disease. To shed light on this complex relationship, scientists have embarked on a journey to explore the biogeographic variation and functional pathways of the gut microbiota in individuals with celiac disease. One challenge researchers face is the variability in sampling sites within the digestive system. Celiac disease primarily affects the small intestine, specifically the duodenum. Therefore, understanding the microbiota along different sections of the duodenum and comparing it to fecal samples is crucial for interpreting the findings accurately and gaining mechanistic insight. Comprehensive Study Using 16S rRNA Gene Sequencing To tackle this issue, a team of scientists conducted a comprehensive study using 16S rRNA gene sequencing, a method that allows for the identification and characterization of microbial communities, and predicted gene function using advanced bioinformatics tools. The research team included Marco Constante; Josie Libertucci; Heather J. Galipeau; Jake C. Szamosi; Gaston Rueda; Pedro M. Miranda; Maria Ines Pinto-Sanchez; Carolyn M. Southward; Laura Rossi; Michelle E. Fontes; Fernando G. Chirdo; Michael G. Surette; Premysl Bercik; Alberto Caminero; and Elena F. Verdu. They are variously affiliated with the Department of Medicine, Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; and the Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas, Instituto de Estudios Inmunológicos y Fisiopatológicos, Universidad Nacional de La Plata-National Scientific and Technical Research Council, La Plata, Argentina. Their team collected duodenal biopsies from sections D1, D2, and D3, aspirates, and stool samples from individuals with active celiac disease, as well as healthy controls. They also assessed participants' celiac disease risk genotypes. To delve deeper into the functional impact of the microbiota, the team selected a subset of duodenal samples with similar celiac disease risk genotypes for further analysis, and used to colonize germ-free mice, enabling the study of gluten metabolism. Study Results - Certain Microbes Present in Celiacs The results of the study were intriguing. The composition and predicted function of the gut microbiota in celiac disease were found to be largely determined by the location within the intestine. In the duodenum, but not in stool samples, specific bacterial species, such as Escherichia coli (D1), Prevotella salivae (D2), and Neisseria (D3), were found to be more abundant in individuals with celiac disease compared to healthy controls. Furthermore, the researchers discovered alterations in bacterial protease and peptidase genes, indicating changes in gluten degradation pathways specific to celiac disease. Interestingly, impaired gluten degradation was observed only in mice colonized with microbiota from individuals with celiac disease, further highlighting the role of the microbiota in gluten metabolism. These findings suggest that celiac disease influences the microbial communities in distinct niches within the gut. The researchers also identified novel microbial proteolytic pathways involved in gluten detoxification, which were impaired in individuals with celiac disease but not in healthy controls carrying the celiac disease risk genotype DQ2. This suggests a potential association between these pathways and active inflammation in the duodenum. It is important to note that the study highlights the significance of sampling site as a confounding factor in microbiome research related to celiac disease. Understanding the nuances of the gut microbiota at different locations within the intestine is crucial for accurate interpretation and meaningful conclusions. Conclusions This groundbreaking research opens up new avenues for exploring the complex interplay between the gut microbiota and celiac disease. By identifying specific microbial species and functional pathways associated with the disease, scientists are gaining valuable insights into its mechanisms. Furthermore, these findings provide potential targets for future therapeutic interventions and diagnostic approaches, ultimately improving the lives of individuals living with celiac disease. As our understanding of the intricate relationship between the gut microbiota and celiac disease deepens, we move one step closer to understanding the parameters of the disease, and possibly to develop better approaches to treatment. Stay tuned for more on this and related stories. Read more at Gastroenterology

Celiac.com 03/06/2023 - We get a lot of questions about celiac disease and gluten-free-related issues. One question we've seen lately is: Is there a connection between the human gut microbiome and celiac disease? The short answer is yes. The longer answer is that research has show a number of connections between the two conditions, but we still have far more questions than answers. Here's a rundown of what we do know. Celiac disease is an autoimmune disorder that affects the small intestine. When individuals with celiac disease consume gluten, a protein found in wheat, barley, and rye, it triggers an immune response that damages the lining of the small intestine and interferes with the absorption of nutrients. One of the key components of the gut environment is the microbiome, a complex community of microorganisms that live in the gut. Recent research has shown that the gut microbiome plays a crucial role in the development and progression of celiac disease. Studies have shown that celiac disease is associated with changes in the composition and diversity of the gut microbiome. In individuals with celiac disease, there is a decrease in beneficial bacteria, such as Lactobacillus and Bifidobacterium, and an increase in pathogenic bacteria, such as Clostridium. This disruption of the gut microbiome, also known as dysbiosis, can lead to an imbalance in the gut environment, which can trigger an immune response and further damage to the small intestine. Celiac Disease Disrupts the Gut Microbiome Recent studies have shown that celiac disease not only affects the gut lining but also disrupts the balance of the gut microbiome. The gut microbiome is made up of trillions of microorganisms that reside in the gut and play a crucial role in maintaining overall health. In healthy individuals, the gut microbiome is diverse and balanced, but in celiac patients, the gut microbiome is often imbalanced, known as dysbiosis. Gluten-Free Diet Affects Gut Microbiome Dysbiosis in celiac patients can lead to a reduction in beneficial bacteria and an increase in harmful bacteria. This can cause a number of issues such as inflammation, changes in gut motility and nutrient malabsorption. Additionally, research has shown that the gut microbiome in celiac patients also changes after starting a gluten-free diet. For instance, the levels of certain beneficial bacteria such as Lactobacillus and Bifidobacterium increase, which can help to restore balance in the gut microbiome. Gut-Brain Axis It is not entirely clear yet how the gut microbiome is affected in celiac disease, but researchers believe that the gut-brain axis, which connects the gut and the brain, plays a key role. Studies have shown that the gut microbiome can influence the brain-gut axis and may impact nociceptive behavior and brain function. There's also a connection between gut-brain axis and migraines in people with celiac disease. Connections Between Microbiome and Celiac Research We also know that Genetic Risk for Autoimmune Disease Tied to Gut Microbiome We know that Celiac Disease Onset Changes Gut Microbiota in Children Recent research shows that Gluten Does Not Change Gut Microbiome in Patients with Celiac Disease and Non-Celiac Gluten Sensitivity We just recently learned that Altered Gut Bacteria Linked With Long COVID-19 Symptoms We also know that, in some cases, Fecal Microbiota Transplant Restores Gut Microbiome New research tells us that interaction between the gut microbiome and micronutrients are a key to the availability of minerals and vitamins. Gut Microbiome Affects Bioavailability of Micronutrients The gut microbiome can variously influence the bioavailability of micronutrients, as well as be influenced by micronutrient supplementation, with potential implications for health, even in the long term. Although several mechanisms have been advanced, a thorough characterization of the microbiome–micronutrient bidirectional axis is of utmost importance, as it can guide the design of microbiome‐based precision intervention strategies, aimed at improving micronutrient status and overall health. Studies have shown that celiac disease is associated with changes in the composition and diversity of the gut microbiome, which can lead to an imbalance in the gut environment, known as dysbiosis. Gut microbiome imbalance can lead to a number of issues such as inflammation, changes in gut motility and nutrient malabsorption. Research has shown that the gut microbiome in celiac patients also changes in some worrisome ways after starting a gluten-free diet. Much Unknown About "Healthy" Gut Microbiome Additionally, we need a clear understanding of what constitutes a "healthy" gut microbiome in people with or without celiac disease to fully understand the implications of gut health on celiac disease. When it comes to the connection between the human gut microbiome and celiac disease, we're learning that the two conditions are connected. Some evidence suggests that the health of the gut microbiome can influence certain symptoms of celiac disease, especially headaches. However, much more research is needed before we can make any hard conclusions about the exact nature of the connections, and the implications for people with celiac disease and other auto-immune conditions.

Celiac.com 02/20/2023 - Celiac disease is a condition that is caused by the immune system's response to gluten, a protein found in wheat, rye and barely. In celiac patients, an immune response triggers a pro-inflammatory environment in the small intestine, causing damage to the tissue. A major role in the pathogenesis of celiac disease is played by the HLA-restricted gliadin-specific intestinal T-cell response generated in a pro-inflammatory environment. A recent review article highlights the growing body of research that supports the central role of inflammation in the development of celiac disease, and how it is influenced by factors such as sensitivity to gluten and other pro-inflammatory agents. The review is authored by researchers Maria Vittoria Barone, Renata Auricchio, Merlin Nanayakkara, Luigi Greco, Riccardo Troncone, and Salvatore Auricchio. The are variously affiliated with the Department of Translational Medical Science, University Federico II in Naples, Italy; and the European Laboratory for the Investigation of Food Induced Disease (ELFID), University Federico II in Naples, Italy. Live studies on a population at risk have explored the mechanisms behind this inflammation. These studies show cellular and metabolic alterations in the absence of a T cell-mediated response, before the onset of the disease and before the introduction of gluten in the diet. Gluten exacerbates these constitutive alterations, both live and in the lab. The role of inflammation in celiac disease has led researchers to consider it as a chronic inflammatory disease, similar to other autoimmune disorders. The review also explores the crucial role played by the intestine in controlling inflammation both locally and systemically, and the impact of nutrients and gut bacteria on inflammation. Reduction of Early Inflammation Could Delay Onset of Celiac Disease Celiac disease is characterized by inflammation, which plays a critical role in the onset of the disease. It begins with a pre-clinical phase where the body is set up for inflammation, making it susceptible to various pro-inflammatory agents, including gluten. Historically, research has focused on the T-cell response in celiac disease, but there is growing recognition of the importance of the pre-inflammatory state. Modulating this state with a Mediterranean-type diet or preventing intestinal viral infections could have a significant impact on the onset of celiac disease, and could be easier to manage than the more complex autoimmune response. The implications of this research extend to additional chronic inflammatory diseases including inflammatory bowel diseases and diabetes, where early intervention with the state of inflammation in at-risk subjects could have a lasting impact on their health. Read more in mdpi.com

Celiac.com 10/17/2022 - Headache is one of the main clinical symptoms and complaints of people with celiac disease, and often it manifests as migraine. The roots and origins of migraine as it relates to celiac disease are complex, and still poorly understood. The term 'dysbiosis' refers to a disruption of the microbiome that triggers an imbalance in the gut microbiota, which leads to changes in their functional composition and metabolic activities, or changes to their distribution within the gut microbiome. A team of researchers recently set out to give a narrative summary of the literature on celiac disease's neurological symptoms, particularly migraines, and to assess potential connections with dysbiosis. The research team included Hodan Qasim, Mohamed Nasr, Amad Mohammad, Mosab Hor, and Ahmed M. Baradeiya. They are variously affiliated with theDepartment of Internal Medicine, Alfaisal University, Riyadh, SAU; the Ophthalmology, Palestinian Medical Council, Ramallah, PSE; the Department of Ophthalmology, Children Retina Institute, Los Angeles, USA; the department of General Internal Medicine, Mansoura general hospital in Mansoura, Egypt; and the Research center, Fresno clinical research center, Fresno, USA. In an effort to explain the connection, researchers have proposed various mechanisms involving the gut-brain axis, including: the interaction of chronic inflammation with inflammatory and vasoactive mediators; the modulation of the intestinal immune environment of the microbiota; and a malfunction of the autonomic nervous system. The research article refers to a known gut-brain pathway that can influence neurological illnesses such as migraines. Some data suggests that gut microbiota can influence the brain-gut axis, and may impact nociceptive behavior and brain function A layer of columnar intestinal epithelial cells separates the 100 trillion bacteria present on the gut surface from the host. The key pathophysiological processes connected to migraine are thought to work partly due to the gut microbiota composition, which also plays a significant role in the gut-brain axis. Potential pathways include neurotransmitters, hormones, and inflammatory chemicals originating from the microbiome. However, further research is required to fully understand the basic specific factors which influence the process. The team's review aims to give a narrative summary of the literature on celiac disease's neurological symptoms, particularly migraines, and to assess any potential associations to dysbiosis, an imbalance in the microbiome that may be related to celiac disease. Read more at Cureus.com

Celiac.com 12/28/2018 - Beyond a few teaser studies, we don’t know enough about whether the individual micro-biome might play a role in the development of celiac disease and inflammatory bowel disease. Top celiac researcher Alessio Fasano, together with colleague G. Serena, recently presented an overview of current knowledge regarding the contribution of the individual micro-biome to celiac disease and inflammatory bowel disease. Their discussion includes a particular focus on how probiotics may be used as potential preventive therapy for CIDs. They are both affiliated with the Mucosal Immunology and Biology Research Center and Division of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital for Children - Harvard Medical School, Boston, MA, USA. As part of their presentation, they write that, globally, cases of chronic inflammatory diseases (CIDs) are undergoing a steep rise. This rise, together with limited effective strategies for slowing these disease explosions demands deeper knowledge of their physical mechanisms in order to reduce the adverse effects of the diseases on children. Several cross-sectional studies have shown a connection between intestinal microbial imbalance and active disease. Unfortunately, they note, these studies do not demonstrate any connection between changes in microflora as a factor in disease development, and so do not suggest any promising directions to explore for possible treatments. Fasano and Serena say that additional studies are needed to show conclusively whether intestinal dysbiosis plays a part in triggering CIDs. Furthermore, given the complexity of the microflora interaction with the host, it is necessary to design a systems-level model of interactions between the host and the development of disease by integrating micro-biome, metagenomics, metatranscriptomics, and metabolomics with either clinical or environmental data. In their overview, Fasano and Serena discuss the current knowledge regarding the contribution of the individual microbiome to celiac disease and inflammatory bowel disease. Their discussion includes a particular focus on how probiotics may be used as potential preventive therapy for CIDs. The article includes a paywall, but you may find it at: Adv Exp Med Biol. 2018 Dec 20. doi: 10.1007/5584_2018_317

Celiac.com 11/26/2020 - For all that recent research has told us about celiac disease, we still don't know whether changes in the intestinal microbiota of children with celiac disease contribute to the disease, or if they are a result of disease and/or its treatment with a gluten-free diet. A team of researchers recently conducted a study to better understand the issue. The research team included Konstantina Zafeiropoulou, Ben Nichols, Mary Mackinder, Olga Biskou, Eleni Rizou, Antonia Karanikolou, Clare Clark, Elaine Buchanan, Tracey Cardigan, Hazel Duncan, David Wands, Julie Russell, Richard Hansen, Richard K. Russell, Paraic McGrogan, Christine A. Edwards, Umer Z. Ijaz, and Konstantinos Gerasimidis. They are variously affiliated with the Human Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, Scotland; the Department of Paediatric Gastroenterology, Royal Hospital for Children, Glasgow, Scotland, UK; and with the department of Civil Engineering, School of Engineering, University of Glasgow, Glasgow, Scotland, UK. The team assessed fecal samples from 57 healthy children, 20 children with new-onset celiac disease, 45 with celiac disease on a gluten-free diet, and 19 unaffected siblings of children with celiac disease in Glasgow, Scotland. The team used 16S ribosomal RNA sequencing to analyze samples, and gas chromatography to measure diet-related metabolites and looked at fecal samples from 13 children with new-onset celiac disease after 6 and 12 months on a gluten-free diet. They then assessed the connections between diet composition, microbiota, gastrointestinal function, and biomarkers of gluten-free diet compliance. Microbiota diversity was similar among the groups. The team saw no microbial dysbiosis in children with new-onset celiac disease. Most of the variation in microbiota composition was explained by the gluten-free diet. The difference in taxa between the groups was about a 3% to 5%, and celiac disease was marked by a specific microbe signature of eleven distinctive operational taxonomic units with high diagnostic probability. About 75% to 94% of the relevant differences between patients on a gluten-free diet with new-onset celiac disease vs healthy children were associated with nutrients and foods, and with biomarkers of gluten ingestion. Meanwhile, fecal levels of butyrate and ammonia decreased with a gluten-free diet. A number of the differences in the gut microbiota of children with established celiac disease appear to result from a gluten-free diet. Meanwhile, it's clear from the data that specific bacteria serve a distinct biomarkers of celiac disease. Further study will help to determine whether these bacteria contribute to celiac disease development. Read more in Gastroenterology

Celiac.com 04/27/2020 - Recent studies on celiac disease have reported changes in the gut microbiome. Researchers don't currently know if the change in the microbial makeup is the cause or a result of the disease, especially in cases of adult onset celiac disease. A team of researchers recently set out to compare of small gut and whole gut microbiota of first-degree relatives with adult celiac disease patients and controls. The research team included Rahul Bodkhe, Sudarshan A. Shetty, Dhiraj P. Dhotre, Anil K. Verma, Khushbo Bhatia, Asha Mishra, Gurvinder Kaur, Pranav Pande, Dhinoth K. Bangarusamy, Beena P. Santosh, Rajadurai C. Perumal, Vineet Ahuja, Yogesh S. Shouche, and Govind K. Makharia. They are variously affiliated with the National Centre for Microbial Resource, National Centre for Cell Science, Pune, India; the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India; the Department of Transplant Immunology and Immunogenetics, All India Institute of Medical Sciences, New Delhi, India; and AgriGenome Labs Pvt. Ltd., Kerala, India. First-degree relatives of celiac patients might offer researchers a chance to study gut microbiome in pre-disease state, since they are genetically prone toward celiac disease. 16S rRNA gene sequencing showed that ecosystem diversity was similar for the disease condition in celiacs, the pre-disease condition in first-degree relatives, and for control subjects. They did note differences in levels of amplicon sequence variant (ASV), indicating changes in specific ASVs between pre-disease and diseased condition. Duodenal biopsies showed greater differences in ASVs compared to fecal samples, which suggests more widespread disturbance to the microbiota in the diseased area. The duodenal microbiota of first-degree relatives was marked by large quantities of ASVs of the genera Parvimonas, Granulicatella, Gemella, Bifidobacterium, Anaerostipes, and Actinomyces. The duodenal microbiota of people with celiac disease contained more ASVs from genera Megasphaera and Helicobacter compared to the microbiota of first-degree relatives. Compared to control group microbiota, the fecal microbiota of both celiacs and first-degree relatives had lower amounts of ASVs classified as Akkermansia and Dorea. Moreover, functional metagenome projections showed reduced gluten degradation by celiac fecal microbiota as compared with first-degree relatives and control subjects. The data show clear differences in ASVs and suggests that celiac fecal microbiota have an impair ability to break down gluten compared to the fecal microbiota of first-degree relatives. More research is needed to examine strain levels and active functional microbiota profiles, in celiacs and first-degree relatives, in order to clarify role of gut microbiome in celiac disease development. Read more in Frontiers of Microbiology, 08 February 2019

Celiac.com 07/25/2018 - Several recent research articles have emphasized the connection between intestinal autoimmune diseases, such as Crohn's disease with dysbiosis or an imbalance in the microbiota composition in the gut. However, little is known about the role of the microbiota in autoimmune pathologies affecting other tissues than the intestine. A team of researchers recently set out to examine the role played by gut microbiota in the pathogenesis of non-intestinal autoimmune diseases, such as Grave's diseases, multiple sclerosis, Type-1 diabetes, systemic lupus erythematosus, psoriasis, schizophrenia, and autism spectrum disorders. They wanted to see if microbiota can influence and determine the function of cells of the immune system. In their report, the team discusses how metabolites derived from bacteria could be used as potential therapies for non-intestinal autoimmune diseases. The report was reviewed by Richard Eugene Frye of Phoenix Children's Hospital, United States, and Matej Oresic at the University of Turku in Finland. The report was edited by Marina I. Arleevskaya of Kazan State Medical Academy in Russia. The authors conclude: "The current evidence supports the notion that changes or alterations of the microbial species that form part of the intestinal microbiota will affect the balance of Tregs and Th17 cells at the intestine, which could modify the immune response of non-intestinal autoimmune diseases. The experimental evidence suggesting that the cytokines secreted from Treg and Th17 will determine and influence non-intestinal autoimmune responses. It could also be possible that cells of the immune system located at the intestine could to move other organs to establish or modify an autoimmune response. The major message of this review is that the abundant data support the notion that the intestine is a critical organ the appropriate immune balance and for the prevention of non-intestinal autoimmune diseases. The key point is that by modifying the intestinal microbiota of a patient that suffers non-intestinal autoimmune disease it might be possible to improve the outcome of such illness." For more on the role of microbiota in influencing immune cell function and promoting individual wellbeing, read the full report in Frontiers in Microbiology. The research team included Maria C. Opazo, Elizabeth M. Ortega-Rocha, Irenice Coronado-Arrázola, Laura C. Bonifaz, Helene Boudin, Michel Neunlist, Susan M. Bueno, Alexis M. Kalergis, and Claudia A. Riedel. They are variously affiliated with the Laboratorio de Biología Celular y Farmacología, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas, Millennium Institute on Immunology and Immunotherapy, Universidad Andres Bello, Santiago, Chile; Facultad de Medicina, Millennium Institute on Immunology and Immunotherapy, Universidad Andres Bello, Santiago, Chile; Laboratorio de Inmunobiología, Facultad de Medicina, Departamento de Biología Celular y Tisular, Universidad Nacional Autónoma de México, Mexico City, Mexico; Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Millennium Institute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile, Santiago, Chile; Unidad de Investigación Médica en Inmunoquímica Hospital de Especialidades Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico; Institut National de la Santé et de la Recherche Médicale U1235, Institut des Maladies de l'Appareil Digestif, Université de Nantes, Nantes, France; and the Departamento de Endocrinología, Facultad de Medicina, Pontificia Universidad, Metropolitana, Chile.

Celiac.com 02/01/2017 - More and more evidence shows a connection between gut inflammation and type 1 diabetes (T1D). A team of researchers recently set out to assess gut inflammatory profiles and microbiota in patients with T1D, and to compare them with healthy controls (CTRL) and with celiac disease patients as gut inflammatory disease controls. The research team included Silvia Pellegrini, Valeria Sordi, Andrea Mario Bolla, Diego Saita Roberto Ferrarese, Filippo Canducci, Massimo Clementi, Francesca Invernizzi, Alberto Mariani, Riccardo Bonfanti, Graziano Barera, Pier Alberto Testoni, Claudio Doglioni, Emanuele Bosi, and Lorenzo Piemonti. They are affiliated with the Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute in Milan, Italy. The team evaluated inflammatory status and microbiome composition in biopsies of the duodenal mucosa from 19 patients with T1D, 19 with celiac disease, and 16 healthy control subjects, recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. They assessed inflammation by gene expression study and immunohistochemistry and used 16S rRNA gene sequencing to analyze microbiome composition. Compared to CTRL and celiac disease patients, the team found an increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα and VEGFA genes in T1D patients. The immunohistochemical analysis confirmed T1D specific inflammatory status was mainly marked by increased monocyte/macrophage lineage infiltration, compared to healthy and celiac disease control tissues. The T1D duodenal mucosal microbiome also proved to be different from the control groups. This was mainly marked by increased Firmicutes, and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the excess of specific bacteria in duodenum. This study shows that patients with T1D show specific abnormalities in gut inflammation and microbiota. Greater knowledge of the complex pathogenesis of T1D will likely provide new directions for therapies targeting the gut. Look for more studies in this area in the near future, as scientists look to nail down specific treatments to prevent gut inflammation. Source: The Journal of Clinical Endocrinology & Metabolism. DOI: https://doi.org/10.1210/jc.2016-3222

Celiac.com 09/16/2016 - Great news about poop transplants: They work! And now doctors kind of understand how and why they work. This is good news about a humor provoking, but very serious matter. Clostridium difficile infection is one of the most common health care-associated infections, and up to 40% of patients suffer from recurrence of disease following standard antibiotic therapy. C. difficile infection has proven to be very difficult to treat. Fecal microbiota transplantation (FMT) has been successfully used to treat recurrent C. difficile infection. Doctors hypothesize that FMT promotes recovery of a microbiota capable of colonization resistance to C. difficile. However, they didn't really understand how it worked. Recently, a research team investigated changes in the fecal microbiota structure following FMT in patients with recurrent C. difficile infection, and imputed a hypothetical functional profile based on the 16S rRNA profile, using a predictive metagenomic tool. After FMT, they also noted increased relative abundance of Bacteroidetes and decreased abundance of Proteobacteria. The research team included Anna M. Seekatz, Johannes Aas, Charles E. Gessert, Timothy A. Rubin, Daniel M. Saman, Johan S. Bakken, and Vincent B. Young. They are variously affiliated with the Department of Internal Medicine, Division of Infectious Diseases, Department of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA; Essentia Health, Department of Gastroenterology, Duluth, Minnesota, USA; Essentia Institute of Rural Health, Duluth, Minnesota, USA; and St. Luke's Hospital, Section of Infectious Diseases, Duluth, Minnesota, USA. Their results showed that, after transplantation, fecal microbiota of recipients was more diverse, and more similar to the donor profile, than the microbiota before transplantation. Additionally, they observed differences in the imputed metagenomic profile. In particular, amino acid transport systems were over-represented in samples collected prior to transplantation. These results Indicate that functional changes accompany microbial structural changes following this therapy. Further identification of the specific microbiota, and functions that promote colonization resistance, may help to create better treatment methods for C. difficile infection. Source: mBio. 2014 May-Jun; 5(3): e00893-14. Published online 2014 Jun 17. doi: 10.1128/mBio.00893-14. PMCID: PMC4068257