Hospital cross-infections and their control

Smith, HC; Loosli, Clayton G.

doi:10.1016/s0022-3476(52)80304-x

Cited by 3 publications

(1 citation statement)

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“…A clinical appreciation for the protective functions of the gastrointestinal microbiota began in the 1940s and 1950s with the rapid introduction of antibiotics for the treatment of bacterial infections (97). Alongside the profound success of antibiotic therapies came the observation that patients often became susceptible to secondary bacterial infections after antibiotic treatment of a primary infection, implicating an unperturbed microbiota as a key player in the generation of colonization resistance (98)(99)(100). In an effort to study this phenomenon, Marjorie Bohnhoff at the University of Chicago pioneered the use of a mouse model for the study of microbiota-mediated colonization resistance (6).…”

Section: Niche Modification By Microbiota-derived Short-chain Fatty A...mentioning

confidence: 99%

Salmonella versus the Microbiome

Rogers

Tsolis

Bäumler

2021

Microbiol Mol Biol Rev

132

105

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SUMMARYA balanced gut microbiota contributes to health, but the mechanisms maintaining homeostasis remain elusive. Microbiota assembly during infancy is governed by competition between species and by environmental factors, termed habitat filters, that determine the range of successful traits within the microbial community. These habitat filters include the diet, host-derived resources, and microbiota-derived metabolites, such as short-chain fatty acids. Once the microbiota has matured, competition and habitat filtering prevent engraftment of new microbes, thereby providing protection against opportunistic infections. Competition with endogenous Enterobacterales, habitat filtering by short-chain fatty acids, and a host-derived habitat filter, epithelial hypoxia, also contribute to colonization resistance against Salmonella serovars. However, at a high challenge dose, these frank pathogens can overcome colonization resistance by using their virulence factors to trigger intestinal inflammation. In turn, inflammation increases the luminal availability of host-derived resources, such as oxygen, nitrate, tetrathionate, and lactate, thereby creating a state of abnormal habitat filtering that enables the pathogen to overcome growth inhibition by short-chain fatty acids. Thus, studying the process of ecosystem invasion by Salmonella serovars clarifies that colonization resistance can become weakened by disrupting host-mediated habitat filtering. This insight is relevant for understanding how inflammation triggers dysbiosis linked to noncommunicable diseases, conditions in which endogenous Enterobacterales expand in the fecal microbiota using some of the same growth-limiting resources required by Salmonella serovars for ecosystem invasion. In essence, ecosystem invasion by Salmonella serovars suggests that homeostasis and dysbiosis simply represent states where competition and habitat filtering are normal or abnormal, respectively.

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