The pathogenesis of inflammatory bowel disease (IBD) is complicated and even several therapeutic strategies have been developed, they are not adequate for achieving mucosal remission in all IBD patients. Several reports have described the role of carbon monoxide (CO) in protection against chronic intestinal inflammation. CO has recently emerged as a potent immunomodulatory entity, anti-inflammatory agent, and homeostasis of physiological condition. CO reduces lipopolysaccharide-induced proinflammatory cytokines in macrophages via the effect of MAPK pathways. Interleukin-6, one of the important cytokines in the pathogenesis of IBD is also regulated by CO. Epithelial cell restitution is reported to be important factor to control IBD and CO has been reported to enhance colonic epithelial restitution through FGF15/19 expression in colonic myofibroblasts. CO also reduced mucosal damage and inflammation in several experimental animal colitis models such as interleukin-10-/- mouse model, TCRα-/- mouse model, dextran sodium sulfate colitis model, and trinitrobennzen sulfonic acid colitis model. Taken together, CO has anti-inflammatory and enhancement of restitution examined in vitro model and in vivo experimental colitis model. These results indicate that CO may have a potential to be one of the therapeutic strategies in IBD patients.
Keywords: Carbon monoxide, cytokine, inflammatory bowel disease, macrophage, restitution, Epithelial cell, trinitrobennzen, anti-inflammatory, pathogenesis, intestinal inflammation
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