Objective To study explores the role of neuromedin U, a neuropeptide derived from sensory nerve terminals, in governing eosinophils (EOS) activation and recruitment in allergic rhinits (AR) mouse model. Methods An AR mouse model was established via intraperitoneal ovalbumin (OVA) sensitization and intranasal challenge, with PBS as a control. Trigeminal ganglion (TG) from AR and control mice were subjected to transcriptomic sequencing to profile differential gene expression. The surgical specimens of AR patients were used for verification, and then the changes of nasal symptoms in AR mice were observed through OVA combined with nasal drip of neurokinin U. EOS proportions in bronchoalveolar lavage fluid (BALF) were quantified using flow cytometry. Bulk RNA sequencing was performed on neuromedin U-treated human peripheral blood-derived EOS to explore the mechanism of action of neurointerin U on EOS. Results Transcriptomic analysis revealed marked upregulation of neuropeptide release pathways in AR mice, with elevated neuromedin U expression in TGs and immunofluorescence-confirmed neuromedin U co-localization with sensory neuronal markers. OVA-challenged mice exhibited significantly higher symptom scores and BALF EOS proportions compared to the controls, which were further amplified by neuromedin U co-administration. Neuromedin U neutralization via anti-neuromedin U antibodies attenuated EOS infiltration. Conclusion Neuromedin U is significantly upregulated in OVA group, and may promote the chemotaxis and adhesion of EOS in AR through the tumor necrosis factor signaling pathway.