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.
Bibliographical noteFunding Information:
This work was supported by grants from the National Research Foundation (NRF) of Korea, funded by the Korean Government (MSIP), 2014R1A2A2A01002861, 2014R1A4A1008625, 2015M3C9A2054020 and 2014R1A1A1006403. This work was also supported by a grant from the Korean Ministry of Health & Welfare, HI14C1324. We appreciate the assistance of Dr. Byung Kwon Kim (OmicsPia, Inc., Taejun, Korea) for bioinformatics analyses.
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All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Physics and Astronomy(all)