The role of nasal microbiota and type 2 innate lymphoid cells in the pathogenesis of allergic rhinitis

Allergic rhinitis (AR) is a type 2 inflammation-related disease, potentially associated with innate lymphoid cells (ILC2s), nasal microbiota, and autophagy. Mice were divided into control, AR, AR + IL-33, and AR + antibiotic groups(n = 5). ELISA was used to measure IL-4, IL-5, and IL-13, Masson staining to evaluate tissue remodeling, flow cytometry to detect ILC2s and memory ILC2s, 16S rRNA sequencing to analyze nasal microbiota, and Western blot to assess autophagy and mitophagy proteins. Compared with controls, mice in each AR group exhibited more nasal symptoms, enhanced tissue remodeling, and altered microbiota diversity with reduced Proteobacteria and increased Firmicutes. IL-33 further elevated type 2 cytokines in serum and nasal lavage fluid, increased nasal ILC2s and miR-155 expression, but did not affect memory ILC2s. All treatment groups showed increased p62 and LC3II/LC3I ratio, along with decreased FUNDC1 and BNIP3L levels. These findings suggest that AR is characterized by type 2 inflammation, tissue remodeling, and microbial dysbiosis, with IL-33 aggravation. Autophagy and mitophagy dysfunction may contribute to AR pathogenesis. • AR shows type 2 inflammation and tissue remodeling, aggravated by IL-33. • Elevated ILC2s and miR-155 upregulation drive type 2 inflammation. • Nasal dysbiosis: IL-33 group shows reduced Proteobacteria and increased Firmicutes. • Impaired autophagy and mitophagy may contribute to AR pathogenesis.