Natural Protein Can Reverse Fibrosing Strictures in Inflammatory Bowel Disease

Natural Protein Can Reverse Fibrosing Strictures in Inflammatory Bowel Disease
A team of researchers recently found that a particular protein can reverse intestinal fibrosis through inhibition of collagen synthesis. The study, titled “Antifibrogenic Effects of the Antimicrobial Peptide Cathelicidin in Murine Colitis-Associated Fibrosis,” was published in the first issue of American Gastroenterological Association peer-reviewed journal Cellular and Molecular Gastroenterology and Hepatology. Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis, is manifested by chronic inflammation of the gastrointestinal tract with significant morbidity and at times life-threatening complications. The mechanisms by which intestinal fibrosis occurs are poorly understood. However, these patients often present high levels of the transforming growth factor-β1 (TGF-β1) in the mucosa overlying CD strictures compared with nonstrictured gut. Nearly 75 percent of patients with CD undergo surgery due to intestinal fibrosis. Recently, studies found that treatments with anti–tumor necrosis factor α (anti-TNFα) monoclonal antibodies can reduce inflammation but may not prevent or reverse fibrosis in CD patients. Cathelicidin (LL-37 in human and mCRAMP in mice) are antimicrobial proteins with anti-inflammatory features. LL-37 also suppresses collagen synthesis, an important fibrotic response, in dermal fibroblasts. In this regard, Hon Wai Koon and colleagues examined if cathelicidin was able to prevent collagen synthesis and fibrosis in intestinal disease. Using mice models of Crohn’s disease and human colonic fibroblasts (the cells that have as function to synthesize collagen in scars and strictures), they conducted the experiment. They administrated trinitrobenzenesulfonic acid to induce chronic colitis and fibros
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