Figure 2. Microbial products with putative effects on GI motility.

GI motility depends on the complex interaction of multiple cell types including enteric neurons, interstitial cells of Cajal, smooth muscle, and immune cells (e.g., macrophages). Luminal gases mediate GI motility; methane and hydrogen sulfide have inhibitory effects on GI transit potentially due to an effect on smooth muscle cells, and molecular hydrogen increases colonic motility by an unidentified mechanism. Lipopolysaccharide produced by Gram-negative bacteria has been suggested to promote survival of enteric nitrergic neurons and motility through Toll-like receptor 4 signaling. The bacterial metabolite, tryptamine, mimics stimulatory effects on motility of serotonin. Luminal short chain fatty acids such as butyrate and acetate promote GI motility through several mechanisms including direct effects on smooth muscle and production of mucosal 5-HT. Production of microbial products regulating motility depends on the availability of specific dietary compounds. 5-HT, serotonin; 5-HT₄R, serotonin receptor; TLR4, Toll-like receptor 4; ICC, interstitial cells of Cajal; LPS, lipopolysaccharide.