Divergent Roles of < b > < i > miR-3162-3p < /i > < /b > in Pulmonary Inflammation in Normal and Asthmatic Mice as well as Antagonism of < b > < i > miR-3162-3p < /i > < /b > in Asthma Treatment

This study aimed to elucidate the role ofmiR-3162-3p in pulmonary inflammation in normal and asthmatic mice as well as preliminarily explore the potential ofmiR-3162-3p antagomir in asthma treatment. A noninvasive whole-body plethysmograph measured airway responsiveness. Both qRT-PCR and Western blot were used to detect the expression of miRNA, mRNA, or protein. Cells in bronchoalveolar lavage fluid were counted by platelet counting and Wright ’s staining. Inflammatory infiltration and mucus secretion were identified by hematoxylin and eosin and periodic acid-Schiff  staining, respectively. Cytokines in the lungs were detected by ELISA. ThemiR-3162-3p mimic intraperitoneally administered to normal mice decreased β-catenin levels in the lungs without obviously altering the lung histology and cytokine levels. AntagonizingmiR-3162-3p in ovalbumin-induced asthmatic mice effectively alleviated the typical features of asthma, such as airway hyper ­responsiveness, airway inflammation, and Th1/Th2 cytokine imbalance, and concomitantly rescued the total and active β-catenin expression. Collectively, we discovered divergent roles ofmiR-3162-3p in lung inflammation between normal and asthmatic mice. The anti-inflammatory effects of themiR-3162-3p antagomir were comparable to those of glucocorticoid treatment. Our study helped in understanding the contribution of miRNAs to the pathogenesis of asthma.Int Arch Allergy Immunol
Source: International Archives of Allergy and Immunology - Category: Allergy & Immunology Source Type: research