Objective To investigate the epithelial expression of stromal interaction molecule 1 (STIM1)/calcium release-activated calcium channel protein 1(Orail)in airway hyperresponsiveness (AHR) and its role.

Methods The mice were divided into control group, ovalbumin (OVA) group and OVA+sh-STIM1 group, with 12 mice in each group. Except for the control group, the other groups established OVA-induced acute asthma mice models. The OVA+sh-STIM1 group was given sh-STIM1 intranasally for intervention. The expression of STIM1 in lung tissue was checked by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the level of inflammatory factors in mouse bronchoalveolar lavage fluid (BALF). The effects of STIM1 knockdown on contractility and Ca²⁺ influx of airway smooth muscle (ASM) cells in human airway smooth muscle cells (HASMC) were analyzed.

Results STIM1 was mainly expressed in bronchial epithelium, and intranasal administration of sh-STIM1 could relieve AHR and inflammation in mice. In vitro, STIM1 knockdown inhibited the contraction of HASMC cells by blocking Oria1 mediated calcium influx ex vivo.

Conclusion STIM1 in epithelial cells regulates airway smooth muscle contraction and AHR, and its mechanism of action is related to the activation of Oria1-mediated calcium influx.