The role of nasal and gut microbiota in allergic rhinitis: immunomodulation and therapeutic prospects

Allergic rhinitis (AR) is a prevalent immunoglobulin E (IgE)-mediated inflammatory disorder of the nasal mucosa that imposes substantial global health and socioeconomic burdens. The pathogenesis of AR involves complex interactions among epithelial barrier dysfunction, immune dysregulation, and environmental factors. Emerging evidence underscores the critical role of the human microbiota, particularly communities residing in the nasal cavity and gut, in modulating immune homeostasis and susceptibility to AR. Early-life microbial exposure profoundly shapes initial microbiota colonization. Observational and longitudinal studies associate nasal and gut dysbiosis with impaired immune tolerance and an increased risk of AR, although the causal direction of these associations remains incompletely established. At a mechanistic level, microbial communities may influence AR through short-chain fatty acids and other metabolites, epithelial barrier integrity, and an integrated innate/adaptive network comprising type 2 innate lymphoid cells, dendritic cell subsets, Th 1, Th2, Th17, and regulatory T cells, together with epigenetic regulation. Among microbiota-targeted interventions, selected probiotic strains and bacterial lysates show modest, strain- and regimen-specific benefits in some randomized trials, whereas fecal microbiota transplantation remains experimental in AR, with current support extrapolated from other conditions and preclinical models. This review synthesizes current insights into microbiota-AR interactions and their underlying mechanisms, explicitly distinguishing human, preclinical, and mechanistic evidence, and critically appraises the therapeutic potential and limitations of microbiota-targeted strategies for AR prevention and treatment.