<i>Bifidobacterium animalis</i> Subsp. <i>Lactis</i> Bla36 Postbiotics Ameliorate Allergic Rhinitis in Juvenile Mice by Repairing the Mucosal Barrier and Modulating Inflammatory Pathways

This study explored the antiallergic effects and mechanisms of postbiotics from <i>Bifidobacterium animalis</i> subsp. <i>Lactis</i> Bla36 (Bla36), focusing on its lysate (Bla36-L), in cellular and juvenile mouse allergic rhinitis models. In RBL-2H3 cells, Bla36-L inhibited mast cell degranulation (lowering β-Hex and HIS release), downregulated Th2 cytokines (IL-4, IL-6, TNF-α), upregulated IL-10, improved HNEpC tight junction integrity to enhance mucosal barrier function, and regulated the FcεRI pathway to block allergic signaling. Metabolomics showed that Bla36 intervention significantly increased sclareol in RBL-2H3 cells, which may mediate anti-inflammatory effects via glycerophospholipid metabolism and NF-κB/MAPK pathway inhibition. In ovalbumin-induced allergic rhinitis mice, intragastric Bla36 dose-dependently reduced serum IgE (65.60-77.74%), alleviated nasal inflammation, restored epithelium, normalized goblet cells, and reduced infiltrates, with high-dose efficacy and no toxicity. Bla36 postbiotics avoid active probiotic colonization risks, offering safety/stability for pediatric use, and provide an experimental basis for their use in allergic disease prevention/treatment, warranting further clinical translation.