Preventive administration of Bifidobacterium animalis subsp. lactis HEM20–01 attenuates the development of atopic dermatitis-like inflammation in mice, along with gut microbial and succinate alterations

Background Atopic dermatitis (AD) is a chronic inflammatory skin disorder frequently accompanied by gut dysbiosis and neurobehavioral comorbidities, but the microbial metabolites mediating gut–skin crosstalk remain unclear. We investigated whether preventive administration of Bifidobacterium animalis subsp. lactis HEM20–01 attenuates the development of AD-like phenotypes and characterized the accompanying gut microbiome, succinate, intestinal, and behavioral alterations. Methods HEM20–01 was orally administered to NC/Nga mice beginning 2 weeks before house dust mite (HDM) induction and continued throughout the 4-week induction period. Cutaneous and intestinal inflammation were assessed by histology, gene expression, and multiplex cytokine analysis, and behavior by the open field test. Fecal microbiota composition and metabolite profiles were analyzed by 16S rRNA gene sequencing and gas chromatography–time-of-flight mass spectrometry (GC-TOF-MS)-based metabolomics. Exogenous succinate was administered in an independent MC903-induced dermatitis model to test whether succinate can aggravate these responses. Results HDM-induced AD-like mice showed activation of the intestinal succinate receptor 1 (SUCNR1)–tuft cell–IL-25 axis and enrichment of the putative succinate-associated family Rikenellaceae and its genus Alistipes , together with elevated fecal and plasma succinate. Preventive HEM20–01 administration attenuated the development of cutaneous and intestinal inflammatory phenotypes. HEM20-01-treated mice also showed a lower relative abundance of putative succinate-associated taxa (Bacteroidaceae, Rikenellaceae, Christensenellaceae, Bacteroides , and Alistipes ), lower circulating succinate levels, reduced activation of SUCNR1–tuft cell–IL-25-related signaling, and attenuated behavioral and hippocampal serotonergic alterations compared with untreated AD-like mice. In a separate MC903-induced dermatitis model, succinate supplementation exacerbated cutaneous and intestinal inflammation. Conclusions Preventive HEM20–01 administration attenuates the development of AD-like phenotypes and associated behavioral alterations, accompanied by changes in gut microbiome composition, lower circulating succinate, and intestinal inflammatory signaling.