Journal
MUCOSAL IMMUNOLOGY
Volume 12, Issue 1, Pages 1-9Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41385-018-0053-0
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Funding
- Canadian Institute of Health Research (CIHR) Fellowship
- NIH [R01 AI042135, AI095706, U01 AI124275, P30 CA008748]
- NATIONAL CANCER INSTITUTE [P30CA008748] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U01AI124275, R01AI042135, R01AI095706] Funding Source: NIH RePORTER
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The communities of bacteria that reside in the intestinal tract are in constant competition within this dynamic and densely colonized environment. At homeostasis, the equilibrium that exists between these species and strains is shaped by their metabolism and also by pathways of active antagonism, which drive competition with related and unrelated strains. Importantly, these normal activities contribute to colonization resistance by the healthy microbiota, which includes the ability to prevent the expansion of potential pathogens. Disruption of the microbiota, resulting from, for example, inflammation or antibiotic use, can reduce colonization resistance. Pathogens that engraft following disruption of the microbiota are often adapted to expand into newly created niches and compete in an altered gut environment. In this review, we examine both the interbacterial mechanisms of colonization resistance and the strategies of pathogenic strains to exploit gaps in colonization resistance.
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