Bifidobacterium animalis Subsp. Lactis 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 Bifidobacterium animalis subsp. Lactis 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.

allergic rhinitis; dose−response relationship; mast cell degranulation; mucosal barrier; postbiotics.