Background: The dysfunction of airway barriers contributes to the development and/or exacerbations of allergic airway inflammation. A major irritant in smoke, acrolein can affect bronchial asthma by altering tight junction protein. But the impact of acrolein on asthma remains poorly understood.
Objective: The aim of this study was to identify the expression of claudin 4 (Cldn4) and the impact of acrolein on Cldn4 in a mouse model of allergic asthma.
Methods: Using mice sensitized with ovalbumin (OVA) and OVA challenged (OVA sensitized/challenged mice) as well as mice treated with saline and challenged with air, and mice exposed to acrolein 5ppm on days 21-23, The effect of acrolein on Cldn4 was estimated using qRT-PCR, ELISA, immunoblotting, immunohistochemical stain, and confocal imaging.
Results: Lung Cldn4 transcript and protein were significantly increased in OVA mice than in sham mice. Acrolein exposure reduced the increase in inflammatory cytokine levels, airway inflammation, and bronchial hyperresponsiveness in OVA mice. Increased lung Cldn4 transcript and protein in OVA mice were decreased in acrolein exposed mice.
Conclusion: These results indicate that Cldn4 might be involved in protective role in the pathogenesis of bronchial asthma, and acrolein can dysregulate Cldn4.
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2013R1A1A2005465).
Keywords: Tight junction, claudin-4, acrolein, bronchial asthma