What is the central question of this study? The relevance of miR-22-3p has been indicated in asthma, while how its protective role exerted in asthma has not been previously reported. What is the main finding and its importance? Upregulation miR-223 hampered the airway inflammation and release of inflammatory cytokines through blocking the activation of NLRP3/Caspase-1/IL-1β signaling pathway in asthma.
Asthma, a great public health burden, is triggered by inflammatory responses in the airways that are not addressed appropriately by current therapies. This study aims to investigate the regulatory mechanism of microRNA-22-3p (miR-22-3p) on the proliferation of bronchial epithelial cells exposed to lipopolysaccharide (LPS) and expressions of pro-inflammatory cytokines in a murine asthma model challenged by ovalbumin (OVA). We first confirmed the overexpression of miR-22-3p in the murine asthma model and bronchial epithelial cells. miR-22-3p remarkably reversed the decline in bronchial epithelial cell viability, enhancement in apoptosis rate, and release of inflammatory factors induced by LPS. miR-22-3p targeted and conversely regulated NACHT, LRR and PYD domains-containing protein 3 (NLRP3). Overexpression of NLRP3 counteracted the inhibitory effect of miR-22-3p on inflammatory damage in bronchial epithelial cells through activation of caspase-1/IL-1β. In an in vivo model, overexpression of miR-22-3p significantly attenuated airway obstruction and tissue damage in mice. In summary, our study underscores that miR-22-3p serves both as a negative regulator of the NLRP3/caspase-1/IL-1β axis and a protective factor against the inflammatory response, thus standing out a future therapeutic modality for asthma. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

References

PubMed