Metabolic tug-of-war: Microbial metabolism shapes colonization resistance against enteric pathogens

被引：1
作者：
Jones, Katerina [1 ]
de Brito, Camila Bernardo [1 ]
Byndloss, Mariana Xavier [1 ,2 ,3 ]
机构：
[1] Vanderbilt Univ, Med Ctr, Dept Pathol Microbiol & Immunol, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Howard Hughes Med Inst, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Med Ctr, Vanderbilt Inst Infect Immunol & Inflammat, Nashville, TN 37232 USA
来源：
CELL CHEMICAL BIOLOGY | 2025年 / 32卷 / 01期
关键词：
ARYL-HYDROCARBON RECEPTOR; CHAIN FATTY-ACIDS; GUT MICROBIOTA; COMMENSAL BACTERIA; ESCHERICHIA-COLI; HOST; SALMONELLA; IMMUNITY; INFECTION; EXPANSION;
D O I：
10.1016/j.chembiol.2024.12.005
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
A widely recognized benefit of gut microbiota is that it provides colonization resistance against enteric pathogens. The gut microbiota and their products can protect the host from invading microbes directly via microbe-pathogen interactions and indirectly by host-microbiota interactions, which regulate immune system function. In contrast, enteric pathogens have evolved mechanisms to utilize microbiota-derived metabolites to overcome colonization resistance and increase their pathogenic potential. This review will focus on recent studies of metabolism-mediated mechanisms of colonization resistance and virulence strategies enteric pathogens use to overcome them, along with how induction of inflammation by pathogenic bacteria changes the landscape of the gut and enables alternative metabolic pathways. We will focus on how intestinal pathogens counteract the protective effects of microbiota-derived metabolites to illustrate the growing appreciation of how metabolic factors may serve as crucial virulence determinants and overcome colonization resistance.
引用
收藏
页码：46 / 60
页数：15
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