Bifidobacterium Breve Yang08 Alleviates Atopic Dermatitis By Enriching Akkermansia Muciniphila and Inhibiting Neutrophil Extracellular Traps Formation In Mice

Atopic dermatitis (AD) is linked to gut microbiota dysbiosis, yet the mechanisms connecting specific commensals to cutaneous immunoregulation remain elusive. We observed reduced Bifidobacterium breve (B. breve) abundance in AD patients. A new B. breve strain was isolated from human stools and nomenclated as Yang08. In MC903-induced AD-like mouse models, Yang08 outperformed a standard strain, ameliorating disease severity, including reduced ear thickening, epidermal hyperplasia, and mast cell infiltration in a manner dependent on viable bacteria and an intact gut microbiota. Antibiotic-mediated microbiota depletion abrogated its efficacy, while fecal microbiota transfer from Yang08-treated mice conferred protection, confirming microbial remodeling as essential. Metagenomics revealed Yang08 specifically enriched Akkermansia muciniphila, which was required for therapeutic effects in germ-free mice. Mechanistically, Yang08 abolished both neutrophil influx and NET deposition in lesions, with ex vivo experiments showing blunted NETosis capacity. Its therapeutic benefits were reversed by neutrophil depletion, NET degradation, or PAD4 inhibition. Overall, Yang08 alleviates AD by enriching A. muciniphila and inhibiting skin NETosis, emerging as a promising prophylactic candidate prevention for AD prevention.

Akkermansia muciniphila; Bifidobacterium breve; atopic dermatitis; neutrophil; neutrophil extracellular traps.