Abstract
<title>Abstract</title> <p> <bold>Objective:</bold> Olfactory dysfunction (OD) is a common symptom of allergic rhinitis (AR) that significantly impairs quality of life, yet its underlying mechanisms remain unclear. This study investigated the role of olfactory bulb neurogenesis mediated by olfactory ensheathing cells (OECs) in AR-related OD and the regulatory effect of IL-1β. <bold>Methods:</bold> An AR mouse model was established using ovalbumin (OVA), and olfactory function was evaluated by the buried food pellet test (BFPT). Neurogenesis and OEC expression in the olfactory bulb were assessed using immunofluorescence and Western blotting. Microglial activation and IL-1β levels were measured, and their correlation with p75NTR was analyzed. In vitro experiments examined the effects of IL-1β on primary OECs. Additionally, intranasal IL-1β administration was performed in vivo to evaluate its impact on olfactory function and olfactory bulb neurogenesis. <bold>Results:</bold> OVA-induced AR mice exhibited significant olfactory dysfunction. Decreased expression of NeuN and PSA-NCAM indicated impaired neurogenesis in the olfactory bulb, accompanied by reduced OEC expression. Increased microglial activation and elevated IL-1β levels were observed, with IL-1β negatively correlated with OEC markers. In vitro, IL-1β aggravated OEC damage, whereas IL-1 receptor inhibition mitigated these effects. In vivo, intranasal IL-1β induced olfactory dysfunction, reduced OEC numbers, and impaired neurogenesis. <bold>Conclusion:</bold> AR-induced olfactory dysfunction is associated with impaired olfactory bulb neurogenesis and OEC damage, potentially mediated by dysregulation of the IL-1β/IL-1Ra axis. This study highlights a novel mechanism involving IL-1β-mediated OEC injury in AR-related OD, providing new insights into its pathogenesis. </p>