Laminaria japonica extract alleviates fine particulate matter-exacerbated allergic rhinitis by inhibiting NLRP3-mediated pyroptosis and restoring epithelial barrier function

Background Allergic rhinitis (AR) is a common chronic inflammatory disease, and environmental pollution, especially fine particulate matter (PM2.5), is an important exacerbating factor that induces inflammation, disrupts the epithelial barrier, and triggers pyroptosis. Pyroptosis has been shown to play a critical role in epithelial damage and inflammatory responses. Therefore, regulating pyroptosis and repairing the epithelial barrier may provide new strategies for the treatment of AR. Purpose Laminaria japonica has potent anti-inflammatory, antioxidant, and immunomodulatory properties. We investigated the protective effects and mechanisms of Laminaria japonica extract (LJE) on PM2.5-exacerbated AR in mice. Study design and methods The AR model was established in mice by OVA sensitization combined with PM2.5 exposure. After intervention with different doses of LJE, behavioral symptoms, serum IgE levels, cytokine expression in nasal lavage fluid and histopathological changes in nasal, intestinal, and splenic tissues were evaluated. Additionally, the expression of NLRP3 inflammasome-related proteins and epithelial barrier-related proteins was detected. Results LJE significantly alleviated nasal and intestinal symptoms, reduced the levels of anti-OVA IgE and IgG1, pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α and the histopathological damages of nasal, colon and spleen tissues. Also, LJE modulated the balances of Th1/Th2 and Treg/Th17, inhibited NF-κB/MAPK signaling pathway. Furthermore, LJE suppressed NLRP3-mediated pyroptosis by downregulation of caspase-1 p20 and IL-1β and restored epithelial barrier integrity in both nasal and colon tissues via up-regulating the expression of E-cadherin and occludin and down-regulating the expression of N-cadherin. Conclusion LJE may have therapeutic potential for AR by regulating NLRP3-mediated pyroptosis and restoring epithelial barrier integrity through NF-κB/MAPK signaling pathway in allergic responses.