Interactive roles of gut microbiota and gastrointestinal motility in the development of inflammatory disorders

Abstract

Gut microbiota play essential roles in host physiology. The gut microbiota both influence and are influenced by gastrointestinal (GI) motility. Disruption of intestinal homeostasis and alterations of the gut microbiota are considered to contribute to the pathogenesis of several disorders. Patients suffering from inflammatory disorders, such as inflammatory bowel disease (IBD) and non-alcoholic steatohepatitis (NASH), reportedly have prolonged orocecal transit times with small intestinal bacterial overgrowth and alterations of gut microbiota. These forms of dysbiosis have been suggested to elicit distinct intestinal immune responses, increased intestinal permeability and bacterial translocation, thereby contributing to the pathogenesis of IBD and/or NASH. In a recent report, we raised the possibility that a drug affecting GI motility might influence gut microbiota and the development of NASH. Thus, we investigated the effects of the gastroprokinetic agent mosapride citrate (MC) using a methionine-choline deficient (MCD) diet-induced NASH rodent model. MC treatment exerted a protective effect against MCD diet-induced GI transit time delay, diminished lactic acid bacteria and colonic inflammation, thereby ameliorating NASH with reduced serum endotoxin and increased glucagon-like peptiede-1. Recently, the correction of dysbiosis employing probiotics or fecal transplantation has been investigated as a therapeutic strategy for IBD and NASH. Given the interactive functions of gut microbiota and mediators of GI motility, there is possibility that altering GI motility also has potential as a therapeutic strategy.