LncRNA OIP5­AS1 aggravates house dust mite­induced inflammatory responses in human bronchial epithelial cells via the miR­143­3p/HMGB1 axis.

Bronchial asthma poses a serious threat to human health. Previous studies have documented the role of long non­coding 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 Opa­interacting protein 5 antisense RNA1 (OIP5­AS1) in the house dust mite­induced inflammatory response in human bronchial epithelial cells. BEAS­2B cells were treated with Dermatophagoides pteronyssinus peptidase 1 (Der p1) to establish an in vitro model of asthma. OIP5­AS1 expression levels increased in BEAS­2B cells following Der p1 treatment, while microRNA (miR)­143­3p was downregulated. Additionally, the levels of the pro­inflammatory factors tumor necrosis factor­α, interleukin (IL)­6 and IL­8 were measured, and apoptosis was evaluated following OIP5 silencing. OIP5­AS1 knockdown reduced the inflammatory response and apoptosis in BEAS­2B cells. Furthermore, using dual luciferase reporter assays and co­transfection experiments, it was demonstrated that the function of OIP5­AS1 was mediated by miR­143­3p. miR­143­3p overexpression attenuated the Der p1­induced inflammatory response and apoptosis of BEAS­2B cells by targeting high mobility group box 1 (HMGB1). In summary, OIP5­AS1 exacerbated Der p1­induced inflammation and apoptosis in BEAS­2B cells by targeting miR­143­3p via HMGB1.