Bifidobacterium breve HH079 alleviates early-life antibiotic-exposed colon dysbiosis in mice by restoring the gut microbiota and gut barrier function.

Abstract

Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of Bifidobacterium breve HH079 (B. breve HH079) on intestinal dysbiosis associated with early-life antibiotic exposure in pups. The results showed that B. breve HH079 treatment inhibited the proliferation of Pseudomonas and Morganella after antibiotic exposure, but promoted the abundance of Bifidobacterium and Bacteroides and acetate production. Concomitantly, the B. breve HH079 administration resulted in decreased M1 gene (Cd86) and protein (TNF-α, IL-1β, LBP and iNOS) expression and increased M2 macrophage marker (Cd206, IL-10 and Arg1) expression in the colonic macrophages of antibiotic-exposed pups, probably by inhibiting the TLR4/NF-κB pathway. Moreover, there was increased intestinal epithelial tight junction protein (Cldn1 and Ocln) expression and the transcription of marker gene (Lyz2, Igha and Reg3β) normalization involved in innate immunity. The results suggested that the new B. breve HH079 strain could alleviate early-life antibiotic-induced colon dysbiosis by regulating the gut microbiota and promoting acetate production and the subsequent M2 macrophage polarization to recover gut health.