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

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.