Pathogenesis of irritable bowel syndrome--review regarding associated infection and immune activation.

There is increasing evidence regarding the role of immune activation in the etiology of irritable bowel syndrome (IBS), which has been mainly been shown in studies investigating mechanisms of postinfectious IBS (PI-IBS). Exposure to intestinal infection induces persistent low-grade systemic and mucosal inflammation, which is characterized by an altered population of circulating cells, mucosal infiltration of immune cells and increased production of various cytokines in IBS patients. Recent studies have also indicated an increased innate immune response in these patients by evaluating expression and activation of Toll-like receptors (TLRs). These findings suggest that immune activation may play a crucial role in the pathogenesis of IBS. In addition, psychological stress has been reported to be one of the factors that induces immune activation. However, it remains unknown whether immune activation in IBS patients is largely dependent on infectious gastroenteritis and/or psychological stress. Additional studies are necessary to understand the precise mechanism of immune activation and its relationship to the development of IBS.