Prebiotics Enhance Microbiome Recovery Following Antibiotic-Induced Dysbiosis

Antibiotic-induced dysbiosis disrupts gut microbiome diversity and functionality, often leading to negative health outcomes, including reduced short-chain fatty acid production, increased susceptibility to opportunistic pathogens, and an increased number of bacterial colonies exhibiting antibiotic resistance. This study investigates the effects of prebiotics (inulin-type fructans) and probiotic supplementation on microbiome recovery in a murine model. Broad spectrum antibiotics induced near-total microbiome depletion, significantly reducing microbial diversity and metabolite production. Prebiotic supplementation demonstrated superior efficacy during recovery in restoring microbiome diversity (~180 species), improving microbiome diversity metrics, and promoting metabolites, particularly butyrate and valerate, compared to probiotics or unmanipulated recovery. While effective in suppressing opportunistic bacterial growth, probiotics significantly delayed total microbial diversity recovery and resulted in lower diversity metrics (~50 species). However, prebiotic-treated microbiomes exhibited a wider antibiotic resistance profile in culturable bacteria, highlighting prebiotics' unique impact on the resistome. These findings underscore the potential of prebiotics for recovery from gut dysbiosis while emphasizing the need for further research to address safety considerations regarding their impacts on antibiotic resistance. Importance: This study explores the impact of prebiotic vs. probiotic manipulation of the microbiome in an antibiotic-induced dysbiosis mouse model. Our data demonstrate that prebiotics are more efficacious at enhancing total diversity and limiting the expansion of potentially harmful opportunist bacteria. This is the first study to indicate that prebiotics increase the number of culturable bacterial colonies resistant to antibiotics. These results contribute to our understanding of microbiome manipulation to promote health and limit disease.