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Categories: Crohn's Disease

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A study of the genetic variation that makes mice more susceptible to bowel inflammation after a high-fat diet has identified candidate genes which may drive inflammatory bowel disease (IBD) in humans.

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A new study shows the sugar sialic acid, which makes up part of the protective intestinal mucus layer, fuels disease-causing bacteria in the gut. The findings suggest a potential treatment target for intestinal bacterial infections and a range of chronic diseases linked to gut bacteria, including inflammatory bowel disease (IBD), celiac disease, irritable bowel syndrome and short bowel syndrome.

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Probiotics can help maintain a healthy gut microbiome or restore populations of 'good bacteria' after a heavy course of antibiotics. But now, they could also be used as an effective treatment strategy for certain intestinal diseases, such as Crohn's disease. Researchers have developed a microgel delivery system for probiotics that keeps 'good' bacteria safe while actively clearing out 'bad' ones. In mice, the system treated intestinal inflammation without side effects.

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For the first time, cells involved with the communication between stress responses in the brain and inflammation in the gastrointestinal (GI) tract have been identified in animal models. Glial cells, which support neurons, communicate stress signals from the central nervous system (CNS) to the semi-autonomous nervous system within the gastrointestinal (GI) tract, called the enteric nervous system (ENS). These psychological stress signals can cause inflammation and exacerbate symptoms of inflammatory bowel disease (IBD).

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Investigators have identified a genetic variant that increases people's risk of developing perianal Crohn's disease, the most debilitating manifestation of Crohn's disease. The variant generates changes to DNA that lead to a loss of protein function, which in turn, alters how the body recognizes and handles bacteria, making it less effective at fighting infections.

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A new study could help improve personalized medicine approaches in inflammatory bowel disease by understanding how patients with variants in the PTPN2 gene develop IBD.

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Fresh insights into how our bodies interact with the microbes living in our guts suggest that a two-drug combination may offer a new way to treat inflammatory bowel diseases such as Crohn's disease and ulcerative colitis.

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Researchers have succeeded in developing an E. coli-based 'smart microbe' that secretes therapeutic payloads, including antibodies, into the gut. The genetically modified beneficial strain of bacteria blocks intestinal inflammation in a preclinical model of inflammatory bowel disease and has the potential to treat intestinal-based diseases.

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Inflammatory diseases like rheumatoid arthritis have complex disease mechanisms that can differ from patient to patient with the same diagnosis. This means that currently available drugs have little effect on many patients. Using so-called digital twins, researchers have now obtained a deeper understanding of the 'off and on' proteins that control these diseases.

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Psyllium fiber protects against ulcerative colitis and suppresses inflammation by activating the bile acid nuclear receptor, a mechanism that was previously unrecognized, according to a new study.

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A new drug acts like a master reset switch in the intestines. The compound, called FexD, has previously been found to lower cholesterol, burn fat, and ward off colorectal cancer in mice. Now, the team reports that FexD can also prevent and reverse intestinal inflammation in mouse models of inflammatory bowel disease.

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Commonly used drugs that reduce joint inflammation in patients with rheumatoid arthritis also reduce vascular inflammation and cardiovascular risk, finds a new study.

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B cells are critical to the proper functioning of the immune system. However, researchers have shown that they can sometimes do more harm than good, as their numbers greatly increase after bowel damage, preventing the tissue from healing. The results can be of significance to the treatment of inflammatory bowel disease.

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Changes in a single gene open the door for harmful gut bacteria to set off the inflammation that drives Crohn's disease, according to a new study. These findings could one day help doctors better select targeted treatments for patients with this immune disorder. This particular host gene, called AGR2, encodes part of the cell's machinery that helps prepare new proteins properly so that they can help repel 'bad' bacteria. When anything from microbes to inflammatory conditions disrupts this process, protein production gets backed up, stressing the cell. Extremes in the expression of AGR2 -- when it becomes too active or just silent -- are associated with such stress and the cell's response to it, and formed the basis of the study described Nov. 15 in Cell Reports.

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Inflammatory bowel disease is a risk factor for giving birth preterm even when in apparent disease remission, a new study shows. If corroborated, the results may eventually affect recommendations for women with ulcerative colitis who tries to conceive.

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Bacteria in the small intestine adapt dynamically to our nutritional state, with individual species disappearing and reappearing. Researchers have now been able to comprehensively study the bacteria of the small intestine and their unique adaptability for the first time. The findings contribute to a better understanding of intestinal diseases such as Crohn's disease or Celiac disease and to the development of new therapeutic approaches.

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Neurons that sense pain protect the gut from inflammation and associated tissue damage by regulating the microbial community living in the intestines, according to a new study.

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Scientists have identified a protein known as sulfatase-2 that plays a critical role in the damage caused by rheumatoid arthritis. The researchers' discovery sheds new light on the molecular processes that drive inflammation seen in rheumatoid arthritis. It could also someday lead to improved treatment of the disease, which currently has no cure.

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An international consortium of researchers has identified genetic variants in 10 genes that elevate a person's susceptibility to Crohn's disease, a form of inflammatory bowel disease. The findings highlight the causal role of mesenchymal cells in intestinal inflammation, helping to zero in on the genetic roots of inflammatory bowel disease.

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Immunologists have identified an important intermediate step in innate immune defense.