A single gene of a commensal microbe affects host susceptibility to enteric infection

Mi Young Yoon, Kyung Bae Min, Kang-Mu Lee, Yujin Yoon, Yaeseul Kim, Young Taek Oh, Keehoon Lee, Jongsik Chun, Byung-Yong Kim, Seok-Hwan Yoon, Insuk Lee, Chan Yeong Kim and Sang Sun Yoon ()
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Mi Young Yoon: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Kyung Bae Min: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Kang-Mu Lee: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Yujin Yoon: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Yaeseul Kim: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Young Taek Oh: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Keehoon Lee: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine
Jongsik Chun: ChunLab Inc., Seoul National University
Byung-Yong Kim: ChunLab Inc., Seoul National University
Seok-Hwan Yoon: ChunLab Inc., Seoul National University
Insuk Lee: College of Life Science and Biotechnology, Yonsei University
Chan Yeong Kim: College of Life Science and Biotechnology, Yonsei University
Sang Sun Yoon: Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: Abstract Indigenous microbes inside the host intestine maintain a complex self-regulating community. The mechanisms by which gut microbes interact with intestinal pathogens remain largely unknown. Here we identify a commensal Escherichia coli strain whose expansion predisposes mice to infection by Vibrio cholerae, a human pathogen. We refer to this strain as ‘atypical’ E. coli (atEc) because of its inability to ferment lactose. The atEc strain is resistant to reactive oxygen species (ROS) and proliferates extensively in antibiotic-treated adult mice. V. cholerae infection is more severe in neonatal mice transplanted with atEc compared with those transplanted with a typical E. coli strain. Intestinal ROS levels are decreased in atEc-transplanted mice, favouring proliferation of ROS-sensitive V. cholerae. An atEc mutant defective in ROS degradation fails to facilitate V. cholerae infection when transplanted, suggesting that host infection susceptibility can be regulated by a single gene product of one particular commensal species.

Date: 2016
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DOI: 10.1038/ncomms11606

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