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Host-mediated sugar oxidation promotes post-antibiotic pathogen expansion

  • Author(s): Faber, F
  • Tran, L
  • Byndloss, MX
  • Lopez, CA
  • Velazquez, EM
  • Kerrinnes, T
  • Nuccio, SP
  • Wangdi, T
  • Fiehn, O
  • Tsolis, RM
  • Bäumler, AJ
  • et al.

Published Web Location

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939260/
No data is associated with this publication.
Abstract

© 2016 Macmillan Publishers Limited. All rights reserved. Changes in the gut microbiota may underpin many human diseases, but the mechanisms that are responsible for altering microbial communities remain poorly understood. Antibiotic usage elevates the risk of contracting gastroenteritis caused by Salmonella enterica serovars1, increases the duration for which patients shed the pathogen in their faeces, and may on occasion produce a bacteriologic and symptomatic relapse2, 3. These antibiotic-induced changes in the gut microbiota can be studied in mice, in which the disruption of a balanced microbial community by treatment with the antibiotic streptomycin leads to an expansion of S. enterica serovars in the large bowel4. However, the mechanisms by which streptomycin treatment drives an expansion of S. enterica serovars are not fully resolved. Here we show that host-mediated oxidation of galactose and glucose promotes post-antibiotic expansion of S. enterica serovar Typhimurium (S. Typhimurium). By elevating expression of the gene encoding inducible nitric oxide synthase (iNOS) in the caecal mucosa, streptomycin treatment increased post-antibiotic availability of the oxidation products galactarate and glucarate in the murine caecum. S. Typhimurium used galactarate and glucarate within the gut lumen of streptomycin pre-treated mice, and genetic ablation of the respective catabolic pathways reduced S. Typhimurium competitiveness. Our results identify host-mediated oxidation of carbohydrates in the gut as a mechanism for post-antibiotic pathogen expansion.

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