LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis.

Abstract

Bronchial asthma poses a serious threat to human health. Previous studies have documented the role of long non-coding RNAs (lncRNAs) in asthma. However, the molecular mechanism underlying bronchial asthma remains unclear. The aim of the present study was to evaluate the role of the lncRNA Opa-interacting protein 5 antisense RNA1 (OIP5-AS1) in the house dust mite-induced inflammatory response in human bronchial epithelial cells. BEAS-2B cells were treated with Dermatophagoides pteronyssinus peptidase 1 (Der p1) to establish an in vitro model of asthma. OIP5-AS1 expression levels increased in BEAS-2B cells following Der p1 treatment, while microRNA (miR)-143-3p was downregulated. Additionally, the levels of the pro-inflammatory factors tumor necrosis factor-α, interleukin (IL)-6 and IL-8 were measured, and apoptosis was evaluated following OIP5 silencing. OIP5-AS1 knockdown reduced the inflammatory response and apoptosis in BEAS-2B cells. Furthermore, using dual luciferase reporter assays and co-transfection experiments, it was demonstrated that the function of OIP5-AS1 was mediated by miR-143-3p. miR-143-3p overexpression attenuated the Der p1-induced inflammatory response and apoptosis of BEAS-2B cells by targeting high mobility group box 1 (HMGB1). In summary, OIP5-AS1 exacerbated Der p1-induced inflammation and apoptosis in BEAS-2B cells by targeting miR-143-3p via HMGB1.