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Host-microbial interactions and regulation of intestinal epithelial barrier function: From physiology to pathology

Author(s): Linda Chia-Hui Yu | Jin-Town Wang | Shu-Chen Wei | Yen-Hsuan Ni

Journal: World Journal of Gastrointestinal Pathophysiology
ISSN 2150-5330

Volume: 3;
Issue: 1;
Start page: 27;
Date: 2012;
Original page

Keywords: Intestinal barrier | Commensal bacteria | Enterocytes | Tight junctions | Lipopolysaccharide | CD14/TLR4 | Inflammatory bowel disease | Colorectal cancer

The gastrointestinal tract is the largest reservoir of commensal bacteria in the human body, providing nutrients and space for the survival of microbes while concurrently operating mucosal barriers to confine the microbial population. The epithelial cells linked by tight junctions not only physically separate the microbiota from the lamina propria, but also secrete proinflammatory cytokines and reactive oxygen species in response to pathogen invasion and metabolic stress and serve as a sentinel to the underlying immune cells. Accumulating evidence indicates that commensal bacteria are involved in various physiological functions in the gut and microbial imbalances (dysbiosis) may cause pathology. Commensal bacteria are involved in the regulation of intestinal epithelial cell turnover, promotion of epithelial restitution and reorganization of tight junctions, all of which are pivotal for fortifying barrier function. Recent studies indicate that aberrant bacterial lipopolysaccharide-mediated signaling in gut mucosa may be involved in the pathogenesis of chronic inflammation and carcinogenesis. Our perception of enteric commensals has now changed from one of opportunistic pathogens to active participants in maintaining intestinal homeostasis. This review attempts to explain the dynamic interaction between the intestinal epithelium and commensal bacteria in disease and health status.

Tango Rapperswil
Tango Rapperswil

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