New clues to the mechanism of inflammatory bowel disease
Inflammatory bowel disease (IBD) describes a group of conditions that involve chronic immune response and inflammation of the gastrointestinal tract. Ulcerative colitis and Crohn disease are the two major types of IBD. It’s estimated that the prevalence for IBD is 396 cases per 100,000 persons annually. The increasing prevalence of IBD creates a considerable burden to individual patients, families as well as the health care system.
Although the exact cause of IBD is not clear, mounting evidence suggests that IBD is a result of the interaction of host genetics, the microbiome, and inflammatory responses. Now a study appearing in Nature Immunity provides new clues to the mechanism of IBD. The study, led by researchers from the University of North Carolina, the University of Michigan, the Columbia University Medical Center, Tel-Aviv University, and Janssen Pharmaceuticals, shows that beneficial bacteria in the gut may be the key to treating IBD.
The researchers previously found that a protein called NLRP12, which is a negative regulator of inflammatory signaling, suppresses inflammation in response to bacterial components, and that it provides protection against colitis, an inflammation of the colon, and colitis-related colon cancer.
For the current study, the researchers further explored the role of NLRP12 in IBD. By analyzing public data of human colitis patients, they noticed that the expression of NLRP12 is reduced in colitis. Experiments in mouse models showed that NLRP12 deficiency increased basal colonic inflammation, which disrupted the balance of the microbiome. NLRP12-deficient mice had less protective bacteria and more harmful bacteria in their gut, and were more susceptible to colitis compared to wide-type mice.
Importantly, the researchers found that these negative effects of NLRP12 deficiency could be reversed by the treatment with antibodies that target inflammatory cytokines or by the administration of beneficial bacteria that normally grow in the gut. Collectively, the results suggest a pivotal role for NLRP12 in keeping the microbiome in balance to prevent inflammation.
In summary, the study reveals that both the absence of NLRP12 and the imbalance of the gut bacteria contribute to the development of IBD. Although there are still many questions, the study may lead to new ways to treat IBD patients who have reduced NLRP12.
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