New Mechanism Underlying Drug Resistance in Crohn’s Disease Identified

New Mechanism Underlying Drug Resistance in Crohn’s Disease Identified
In a new study entitled “Chronic inflammation up-regulates P-gp in peripheral mononuclear blood cells via the STAT3/Nf-κb pathway in 2,4,6-trinitrobenzene sulfuric acid-induced colitis mice,” researchers identified a mechanism underlying drug resistance in Crohn's disease patients. The study was published in the journal Scientific Reports. Inflammatory bowel disease (IBD) is characterized by chronic inflammation in the digestive tract and comprises two main types – Crohn's disease and Ulcerative Colitis. While the pathogenesis of both Crohn's disease and Ulcerative Colitis is still unclear, IBD patients also exhibit significant alterations and dysregulated immune system responses. Because of this, IBD is also characterized as an autoimmune disease. Accordingly, IBD patients’ treatment usually includes immunosuppressive and anti-inflammatory drugs. Increasingly reported, however, is the development of drug resistance in these patients. This resistance is divided into intrinsic resistance (patients present little or no sensitivity to immunosuppressants in the beginning of the treatment) and acquired resistance (patients gradually develop resistance with long-term treatment with immunosuppressant’s). While the mechanisms triggering acquired resistance in IBD patients are known, those underlying intrinsic resistance lack a common agreement among the scientific community, especially for Crohn’s disease. In this new research, the authors used a mouse model of Crohn’s disease, the trinitrobenzene sulfuric acid (TNBS)-induced rat model (a good model exhibiting the same features as human Crohn's disease patients) and analyzed its resistance to therapy by measuring the function and expression of P-glycoprotein (P-gp) in a population of blood immune cell
Subscribe or to access all post and page content.