Intestinal colonization resistance
Open accessAbstract
Summary: Dense, complex microbial communities, collectively termed the microbiota, occupy a diverse array of niches along the length of the mammalian intestinal tract. During health and in the absence of antibiotic exposure the microbiota can effectively inhibit colonization and overgrowth by invading microbes such as pathogens. This phenomenon is called ‘colonization resistance’ and is associated with a stable and diverse microbiota in tandem with a controlled lack of inflammation, and involves specific interactions between the mucosal immune system and the microbiota. Here we overview the microbial ecology of the healthy mammalian intestinal tract and highlight the microbe–microbe and microbe–host interactions that promote colonization resistance. Emerging themes highlight immunological ( T helper type 17/regulatory T ‐cell balance), microbiota (diverse and abundant) and metabolic (short‐chain fatty acid) signatures of intestinal health and colonization resistance. Intestinal pathogens use specific virulence factors or exploit antibiotic use to subvert colonization resistance for their own benefit by triggering inflammation to disrupt the harmony of the intestinal ecosystem. A holistic view that incorporates immunological and microbiological facets of the intestinal ecosystem should facilitate the development of immunomodulatory and microbe‐modulatory therapies that promote intestinal homeostasis and colonization resistance.
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Residents' antimicrobial use can negatively impact their gut, skin, and other body site microbiotas, which normally provide protection against establishment and proliferation of exogenous and potentially pathogenic bacteria, a phenomenon called colonization resistance.
“Specifically, residents' antimicrobial use can negatively impact their gut, skin, and other body site microbiotas, which normally provide protection against the establishment and proliferation of exogenous and potentially pathogenic bacteria, a phenomenon called colonization resistance 26 .”
From Urban informal settlements as hotspots of antimicrobial resistance and the need to curb environmental transmission. (2020) · cites this paper as [26]
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- Authors
- Lawley, T. D., & Walker, A. W.
- Affiliations
- Wellcome Sanger Institute (GB)
- Corresponding author
- Lawley, Trevor D.
- Venue
- Immunology
- Publisher
- Wiley
- Published
- 2012-12-13
- Volume
- 138
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0019-2805 (ISSN-L)
- 1365-2567
- PMC
- PMC3533696
- OpenAlex
- W2012151682
- Cited by
- 610
- References
- 22
- Citations by year
- 2026: 22 · 2025: 49 · 2024: 62 · 2023: 56 · 2022: 54 · 2021: 51 · 2020: 51 · 2019: 54 · 2018: 47 · 2017: 47 · 2016: 27 · 2015: 43 · 2014: 26 · 2013: 18 · 2012: 1
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (076964, 098051)
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Infectious Diseases › Clostridium difficile and Clostridium perfringens research
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Keywords
- gut microbiota, mucosal immunity, microbial ecology, Th17 cells, regulatory T cells, short-chain fatty acids, intestinal inflammation, pathogen virulence factors, antibiotic use, intestinal homeostasis, immunomodulatory therapy, microbial interactions
- MeSH terms
- Animals, Humans, Gastrointestinal Tract, Microbial Interactions
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