Clara cell 16 KDa protein mitigates house dust mite-induced airway inflammation and damage via regulating airway epithelial cell apoptosis in a manner dependent on HMGB1-mediated signaling inhibition

Abstract Background House dust mite (HDM) inhalation can cause airway epithelial damage which is implicated in the process of inflammation asthma. High mobility group box 1 (HMGB1) critically required for cellular and apoptosis as an important endogenous danger signal. Recently, Clara cell 16KDa protein (CC16) has been identified to exert anti-inflammatory immunomodulatory influence various injury-related diseases model. However, little known about its ability protect against injury allergic This study was aimed clarify protective roles CC16 on epithelia HDM-induced asthma regulation HMGB1 by CC16. Methods Mice were sensitized challenged HDM extract administrated intranasally with (5 ?g/g or 10 ?g/g) saline period. The BEAS-2B human line cultured control vehicle then exposed HDM. Knockdown overexpression induced transfection intratracheal injection recombinant adenovirus. Results treatment decreased histological epithelium dose-dependently Airway upon stimulation noticeably abrogated vivo vitro. In addition, upregulation expression related signaling also detected under conditions, while silencing significantly inhibited cells. Furthermore, activity HMGB1-mediated restrained after whereas abolished effect apoptosis. Conclusions Our data confirm that attenuates HDM-mediated via suppressing a HMGB1-dependent manner, suggesting role potential option