Background and aim: miR-29s have been implicated in the modulation of innate immune responses and regulation of IL-33 through soluble ST2 (sST2) release. We aimed to determine the expression of miR-29s and sST2 in bronchial samples from healthy and asthmatic individuals and release of sST2 from bronchial epithelial cells (BECs) treated with asthma-associated triggers and cytokines.

Methods: Expression of ?800miRNAs were assessed in bronchial biopsies from 6 healthy and 6 asthmatic subjects using the NanoString nCounter platform. RT-qPCR was performed to further validate miR-29 expression in 8 healthy and 20 asthmatic subjects. sST2 was measured by ELISA in bronchial lavage (BL) fluid from the same 28 subjects and in supernatants from air-liquid interface cultured primary human BECs (n=3-8) treated with HDM, poly(I:C), IL-4/IL-13 or IL-17.

Results: miRNA profiling in bronchial biopsies identified increased expression of miR-29b-3p (p<0.05) and miR-29c-3p (p<0.05) in asthmatic subjects compared to healthy controls. RT-qPCR analysis confirmed significant upregulation of miR-29b-3p in asthma (p<0.05). Levels of sST2 tended to be lower in BL from asthmatic subjects compared to healthy controls and were reduced in supernatants from HDM-treated BECs (p=0.054).

Conclusion: Our data suggest that bronchial epithelial release of sST2, a decoy receptor for IL-33, is reduced by allergen exposure and that airway sST2 may be decreased in asthma. Since miR-29s are proposed to regulate sST2 expression, elevated levels of bronchial miR-29b-3p in asthma may play a role in exacerbating IL-33-dependent allergic inflammationand warrants further studies.