ERS Respiratory Channel

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Abstract

Background and aim: House dust mites (HDM) induce the generation of reactive oxygen species (ROS) and mitophagy in bronchial epithelial cells. MicroRNAs (miRNAs) have been implicated in immune responses in allergic asthma. In this study, we aimed to determine the role of miRNAs in allergen-induced mitophagy in human bronchial epithelial cells (BEAS-2B).

Methods: The nCounter NanoString miRNA analysis technology was used to determine the miRNA signatures in HDM-treated BEAS-2B cells. ELISA, western blot and RT-qPCR assay were used to define the expression of mitophagy markers and inflammatory cytokines. Biotin-based pull-down assay was applied to identify miR-197-3p target genes. The effects of miR-197-3p on BEAS-2B cells were assessed by overexpressing and silencing techniques, MTS cell proliferation assay, flow cytometer and confocal microscope analysis.

Results: Our data demonstrates that miR-197-3p is significantly downregulated in HDM treated BEAS-2B cells as compared to control cells. miR-197-3p was shown to target the NDP52 mitophagy receptor and IL-13 in BEAS-2B cells. Overexpression of miR-197-3p reduced HDM-induced mitophagy, NF-kB signaling pathway, and the production of ROS, IL-13, IL-8, IL-33, and TSLP. Inhibition of miR-197-3p further increased mitophagy, NF-kB signaling and the production of inflammatory cytokines.

Conclusion: Our data suggest a regulatory role of miR-197-3p in HDM-induced inflammatory responses. Thus, airway epithelial miR-197-3p may play a role in epithelial dysfunction in asthma. However, further studies are needed to confirm the role of miR-197-3p in human primary bronchial epithelial cells.

Abstract

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