Research Uncovers How Gut Microbiota and Genes Worsen Ulcerative Colitis
New research reveals how interactions between gut microbiota and gene mutations, especially in OTUD3, aggravate ulcerative colitis through immune signaling pathways, opening potential for targeted therapies.
Ulcerative colitis (UC) is a chronic inflammatory condition affecting the large intestine, leading to symptoms like abdominal pain, cramping, frequent bowel movements, and bloody diarrhea. The disease often presents with periods of remission followed by sudden flare-ups, and currently, there is no cure available.
A significant factor in UC is the role of the intestinal microbiota, which encompasses the diverse community of microbes residing in the gut. In healthy individuals, this microbiota helps facilitate digestion and supports overall health. However, in UC patients, this microbial community becomes imbalanced, a condition known as dysbiosis. Dysbiosis involves a reduction in beneficial microbes and an increase in harmful ones, contributing to disease progression.
Recent research published in Science Immunology by a team led by Osaka University has shed light on the complex interaction between gut microbes, genetics, and immune signaling pathways in UC. The study focused on how mutations in the OTUD3 gene, alongside dysbiosis, influence the severity of UC. They identified that specific mutations, known as single nucleotide variants (SNPs), in OTUD3 act as risk factors for developing the disease.
The researchers examined the gut microbiota from both healthy individuals and UC patients. When they transplanted these microbiotas into mice models, results showed that only mice with mutant OTUD3 genes developed UC-like symptoms after receiving UC microbiota. This indicated a genetic predisposition that interacts with microbial imbalance.
Further investigation revealed that the STING protein, which is activated by microbes, becomes overactive when OTUD3 mutations are present. This overactivation leads to increased inflammation in the colon. Notably, transplanting UC microbiota into mice lacking the STING gene prevented the development of UC symptoms, confirming the pathway’s central role.
This research highlights that UC arises from a combination of genetic mutations and alterations in the gut microbial environment. Understanding this interplay opens new avenues for targeted therapies. The findings suggest that modulating gut microbiota and inhibiting STING signaling could serve as promising strategies for UC treatment. Ultimately, this study advances our knowledge of the disease mechanisms and may lead to more precise diagnostic and individualized treatment options for UC patients.
Source: Medical Xpress
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