期刊
CURRENT OPINION IN MICROBIOLOGY
卷 64, 期 -, 页码 82-90出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.mib.2021.09.014
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资金
- VFoundation for Cancer Research [V2020-013]
- Vanderbilt Digestive Disease Pilot and Feasibility grant [P30 058404]
- ACS Institutional Research Grant [IRG-19-139-59]
- VICC GI SPORE grant [P50CA236733]
- United States-Israel Binational Science Foundation [2019136]
- NIH Environmental Toxicology T32 Training Grant [T32ES007028-46]
- Howard Hughes Medical Institute through the James H. Gilliam Fellowships for Advanced Study program [GT15104]
- Basic Science Research Program through the National Research Foundation of Korea (NRF) by the Ministry of Education [2020R1A6A3A03037326]
- Direct For Computer & Info Scie & Enginr
- Office of Advanced Cyberinfrastructure (OAC) [2019136] Funding Source: National Science Foundation
- National Research Foundation of Korea [2020R1A6A3A03037326] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The intestine is a complex bacterial ecosystem that provides immune education, nutrition, and protection against pathogens. Symbiotic interactions between the host and microbiome occur through metabolic crosstalk, with microbiota inhibiting pathogen colonization through diverse metabolic pathways, while pathogens disrupt the microbiome to gain a metabolic advantage. This review discusses the role of microbiota metabolites in colonization resistance and the metabolic mechanisms used by pathogens to outcompete commensal microbes.
The intestine is home to a large and complex bacterial ecosystem (microbiota), which performs multiple beneficial functions for the host, including immune education, nutrition, and protection against invasion by enteric pathogens (colonization resistance). The host and microbiome symbiotic interactions occur in part through metabolic crosstalk. Thus, microbiota members have evolved highly diverse metabolic pathways to inhibit pathogen colonization via activation of protective immune responses and nutrient acquisition and utilization. Conversely, pathogenic Enterobacteriaceae actively induce an inflammation-dependent disruption of the gut microbial ecosystem (dysbiosis) to gain a competitive metabolic advantage against the resident microbiota. This review discusses the recent findings on the crucial role of microbiota metabolites in colonization resistance regulation. Additionally, we summarize metabolic mechanisms used by pathogenic Enterobacteriaceae to outcompete commensal microbes and cause disease.
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