Interactions Between Commensal Bacteria and Gut Sensorimotor Function in Health and Disease

Abstract

Commensal bacteria inhabiting the human intestine (i.e., intestinal microflora) participate in the development and maintenance of gut sensory and motor functions, including the promotion of intestinal propulsive activity. On the other hand, intestinal motility represents one of the major control systems of gut microflora, through the sweeping of excessive bacteria from the lumen. There is emerging evidence indicating that changes in this bidirectional interplay contribute to the pathogenesis of gut diseases, such as small intestinal bacterial overgrowth and intestinal pseudo-obstruction. Recent interest has also been directed to the potential role of intestinal microflora in the pathogenesis of the irritable bowel syndrome. Although the status of intestinal microflora in the irritable bowel syndrome remains unsettled, small intestinal bacterial overgrowth (as detected with breath testing) and increased fermentation of foods with gas production, provide indirect evidence that microflora may contribute to symptom generation in irritable bowel syndrome. The potential benefit of antibiotic and probiotic therapy is currently under investigation and opens new perspectives in irritable bowel syndrome treatment.

Mutual reinforcement of pathophysiological host‐microbe interactions in intestinal stasis models

“…Bacterial metabolites directly stimulate gut enteric neurons, intestinal smooth muscle, and enteroendocrine cells that secrete biologically active peptides (Barbara et al. 2005). Colonization of GF mice with microbiota from loperamide‐treated or nontreated mice, as well as from IBS‐C or control patients improves GI transit time, indicating the importance of the microbiome on gut motility.…”

“…2005). For example, dietary intake impacts GI transit time, but can also affect gut microbial community structure and function.…”

Gut barrier disruption by an enteric bacterial pathogen accelerates insulitis in NOD mice

“…Epithelial TLR signalling is critical in maintaining intestinal epithelial integrity [40]. Disruption of this homeostasis as a result of a dysregulated interaction between TLRs and enteric bacteria promotes both inflammatory bowel disease and type 1 diabetes [14,42]. It is possible that enhanced antigen presenting cell-mediated TLR signalling is induced by enteric organisms breaching a gut barrier and that this promotes insulitis.…”

Chronic intestinal pseudo-obstruction

“…Poorly absorbable antibiotics such as paramomicine and rifaximine should be preferred, but alternating cycles with metronidazole and tetracycline are necessary to limit resistances [74] .…”