Chapter 14 : The Roles of Inflammation, Nutrient Availability and the Commensal Microbiota in Enteric Pathogen Infection

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Genetic susceptibility, the mucosal immune system, and environmental factors such as the microbiota, stress, and diet, contribute to the pathogenesis of inflammatory bowel disease (IBD) ( ). Involvement of the microbiota has been proposed early on, as microbiota manipulation by antibiotics or probiotics can treat or alleviate IBD symptoms in humans. In experimental animal models, the gut luminal microbiota is required for the induction of chronic inflammation ( ). Different theories about how the microbiota is involved in the pathogenesis of IBD have been proposed. (1) Mutations that lead to a defective mucosal barrier function (e.g., mucus layer, innate killing, antimicrobial peptides) involve excessive translocation of commensal bacteria and triggering of proinflammatory signalling cascades. (2) Abnormal host immune regulation induces an overshooting immune response against intrinsic commensal bacteria. (3) The presence of an unidentified pathogen leads to induction of the disease or (4), a dysbiotic microbiota, characterized by an imbalance between “beneficial” and “potentially harmful” commensal bacteria, acts as a trigger or driver of the disease. The latter theory has been challenged by studies conducted in experimental rodent models: inflammatory disease conditions in the course of chronic colitis or enteropathogen infection can disrupt normal microbiota composition, induce dysbiosis, and favor overgrowth of pathogens and commensals with an increased virulence potential ( ). Therefore, dysbiosis may not only be considered as a cause but also a consequence of gut inflammation.

Citation: Stecher B. 2015. The Roles of Inflammation, Nutrient Availability and the Commensal Microbiota in Enteric Pathogen Infection, p 297-320. In Conway T, Cohen P (ed), Metabolism and Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MBP-0008-2014
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