Ruminococcus gnavus ameliorates atopic dermatitis by enhancing Treg cell and metabolites in BALB/c mice

Abstract Background Ruminococcus gnavus ( R . gnavus ) are mucin‐degrading gut bacteria that play a key role in the early colonization of the gut by serving as endogenous sources of nutrients. They can also influence immune development. We had previously reported a lower abundance of R . gnavus in infants with atopic dermatitis (AD) compared with that in healthy subjects. However, the underlying mechanisms remain unclear. In this study, we investigated the effect of orally administered R . gnavus on antibiotic treatment‐induced gut dysbiosis (and the underlying mechanism) in a mouse model of AD. Methods Four‐week‐old female BALB/C mice were administered antibiotic cocktails for 2 weeks. R . gnavus was orally administered throughout the study duration. At 6 weeks of age, AD was induced by epidermal sensitization with ovalbumin. AD phenotypes and systemic and gut immune responses were investigated. Results Orally administered R . gnavus significantly reduced AD‐associated parameters (i.e., transepidermal water loss, clinical score, total serum immunoglobulin (Ig) E level, OVA‐specific IgE level, and skin inflammation). R . gnavus treatment also resulted in significant downregulation of T helper 2–related cytokine mRNA and upregulation of interleukin (IL)‐10 and Foxp3 in the skin. The population of CD4 + FOXP3 + T cells in mesenteric‐ and skin‐draining lymph nodes and butyrate levels in the cecum increased in R . gnavus ‐administered AD mice. Conclusions Immune modulation by orally administered R . gnavus may alleviate AD symptoms through the enhancement of regulatory T‐cell counts and short‐chain fatty acids production in AD mice.