Salmonella Typhimurium Diarrhea Reveals Basic Principles of Enteropathogen Infection and Disease-Promoted DNA Exchange

Publication date: 12 April 2017
Source:Cell Host & Microbe, Volume 21, Issue 4
Author(s): Sandra Y. Wotzka, Bidong D. Nguyen, Wolf-Dietrich Hardt
Despite decades of research, efficient therapies for most enteropathogenic bacteria are still lacking. In this review, we focus on Salmonella enterica Typhimurium (S. Typhimurium), a frequent cause of acute, self-limiting food-borne diarrhea and a model that has revealed key principles of enteropathogen infection. We review the steps of gut infection and the mucosal innate-immune defenses limiting pathogen burdens, and we discuss how inflammation boosts gut luminal S. Typhimurium growth. We also discuss how S. Typhimurium-induced inflammation accelerates the transfer of plasmids and phages, which may promote the transmission of antibiotic resistance and facilitate emergence of pathobionts and pathogens with enhanced virulence. The targeted manipulation of the microbiota and vaccination might offer strategies to prevent this evolution. As gut luminal microbes impact various aspects of the host's physiology, improved strategies for preventing enteropathogen infection and disease-inflicted DNA exchange may be of broad interest well beyond the acute infection.

Teaser

Wotzka et al. discuss how normal microbiota, innate mucosal immune responses, and antibodies fend off enteropathogens. Basic principles discovered in Salmonella Typhimurium infection models may be of equal relevance for the co-habitation of the microbiota with their hosts.


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