In summary, we were the first to investigate the expression of Sema3E in lung tissue and vagal ganglion in OVA-sensitized AS and EB models, and found that Sema3E might act as an upstream regulator in the vagal ganglia to regulate AHR and airway eosinophilic inflammation in allergic asthma, which provided new ideas for the follow-up study of the mechanism of AHR in asthma and chronic cough in EB. Here, SEMA3E is linked to epidermolysis bullosa.