| Direct interaction of gut microbiota with pathogenic invader or pathobiont |
Niche exclusion: consumption on same limited resources to eventually out-compete and starve the competing pathogen. Alter ambient oxygen tension: suppress certain microbial virulence and survival Fermentation products (e.g., SCFAs): downregulate pathogens virulence factor; modulating intestinal pH to selectively inhibit microbial growth and promote growth of other microbes. Microbiota-host co-metabolite (e.g., secondary bile acids): antimicrobial property Antibiotic production: selective killing of microbes, modify microbiota composition Antibiotic detoxification (e.g., Beta-lactamase, efflux pump): microbial self-defense mechanism, removal of toxic molecules. Antimicrobial or toxin production (e.g., Bacteriocin): induce specific growth inhibition on members of the same or similar species. |
Cherrington et al., 1991; Britton and Young, 2012; Kamada et al., 2013; McNally and Brown, 2015
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| Gut microbiota-mediated stimulation or enhancement of host defense mechanisms |
Gut microbiota interacts with local pattern recognition receptors (PRRs) such as toll-like receptors (TLRs) and nod-like receptors (NLRs) signaling to facilitate maintenance of intestinal immunity homeostasis. Stimulate production of host antimicrobial peptides (e.g., Defensins). Induce secretion of immunoglobulin A (IgA), pro-inflammatory cytokines: recruitment of immune cells to eradicate pathogens. Induce activation of T helper type 17 (TH17) cells without intestinal pathology, enhancing resistance toward intestinal pathogen. |
Ivanov et al., 2009; Lawley and Walker, 2013; Yiu et al., 2017
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