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Colonization resistance is a critical defensive mechanism provided by the commensal gut microbiota to prevent the invasion and expansion of enteric pathogens such as Clostridioides difficile and Vancomycin-resistant Enterococci (VRE) (Buffie & Pamer, 2013). This protective effect is mediated through several pathways, including direct competition for essential nutrients, the production of antimicrobial molecules like bacteriocins, and the metabolic conversion of primary bile acids into secondary bile acids that inhibit pathogen germination and growth (Kim et al., 2017). Disruption of the gut microbiota, typically by broad-spectrum antibiotics, compromises colonization resistance and creates an ecological opening for opportunistic infections (Ducarmon et al., 2019). Therapeutic interventions, such as fecal microbiota transplantation (FMT) and defined live biotherapeutic products (LBPs) like SER-109, aim to restore this resistance by reintroducing a diverse community of beneficial microbes (FDA, 2023). These treatments help re-establish the metabolic and ecological barriers necessary to suppress pathogens and maintain intestinal health.
Restoration of microbial diversity and ecological niches to suppress pathogen growth through nutrient competition, production of inhibitory metabolites like secondary bile acids and short-chain fatty acids, and induction of host antimicrobial peptides (Buffie & Pamer, 2013; Kim et al., 2017).
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