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Review
. 2017 May 26;292(21):8577-8581.
doi: 10.1074/jbc.R116.752295. Epub 2017 Apr 7.

Colonization resistance: The deconvolution of a complex trait

Affiliations
Review

Colonization resistance: The deconvolution of a complex trait

Erin E Olsan et al. J Biol Chem. .

Abstract

Carbapenemase-producing Enterobacteriaceae are an emerging threat to hospitals worldwide, and antibiotic exposure is a risk factor for developing fecal carriage that may lead to nosocomial infection. Here, we review how antibiotics reduce colonization resistance against Enterobacteriaceae to pinpoint possible control points for curbing their spread. Recent work identifies host-derived respiratory electron acceptors as a critical resource driving a post-antibiotic expansion of Enterobacteriaceae within the large bowel. By providing a conceptual framework for colonization resistance against Enterobacteriaceae, these mechanistic insights point to the metabolism of epithelial cells as a possible target for intervention strategies.

Keywords: Escherichia coli (E. coli); Klebsiella pneumonia; Salmonella enterica; antibiotic resistance; antibiotics; microbiome.

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Conflict of interest statement

M. X. B. and A. J. B. filed invention report number 0577501-16-0038 at iEdison.gov for a treatment to prevent post-antibiotic expansion of Enterobacteriaceae

Figures

Figure 1.
Figure 1.
Antibiotics lower colonization resistance against Enterobacteriaceae. The gut microbiota breaks down complex carbohydrates into a variety of fermentation products, such as butyrate. Butyrate serves as the main energy source for colonocytes, which oxidize this short-chain fatty acid to produce ATP for the absorption of sodium (Na+). This metabolism consumes oxygen (O2) thereby rendering the colonic surface hypoxic (<1% oxygen). Antibiotics deplete butyrate-producing bacteria, which forces colonocytes to switch their metabolism to a fermentation of glucose to lactate, thereby increasing the abundance of nitrate (NO3) and oxygen in the gut lumen. Facultative anaerobic bacteria can use these host-derived electron acceptors to grow better on carbon sources than obligate anaerobic bacteria, which drives a luminal expansion of Enterobacteriaceae.

References

    1. Bohnhoff M., Drake B. L., and Miller C. P. (1954) Effect of streptomycin on susceptibility of intestinal tract to experimental Salmonella infection. Proc. Soc. Exp. Biol. Med. 86, 132–137 - PubMed
    1. Bohnhoff M., and Miller C. P. (1962) Enhanced susceptibility to Salmonella infection in streptomycin-treated mice. J. Infect. Dis. 111, 117–127 - PubMed
    1. Meynell G. G. (1963) Antibacterial mechanisms of the mouse gut. II. The role of Eh and volatile fatty acids in the normal gut. Br. J. Exp. Pathol. 44, 209–219 - PMC - PubMed
    1. Saito K. (1961) Studies on the habitation of pathogenic Escherichia coli in the intestinal tract of mice. I. Comparative experiments on the habitation of each type of resistant pathogenic Escherichia coli under an administration of streptomycin. Paediatr. Jpn. 65, 385–393 - PubMed
    1. Saito K. (1961) Studies on the habitation of pathogenic Escherichia coli in the intestinal tract of mice. II. Experimental inoculation of type 055 Escherichia coli after long-term administration of streptomycin. Paediatr. Jpn. 65, 394–399 - PubMed

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