Long Noncoding RNA HOXA Cluster Anti-Sense RNA 2 Inhibits Mycoplasma pneumoniae-Induced Inflammation by Regulating the Nuclear Factor-KappaB Signaling Pathway

Abstract

Mycoplasma pneumoniae (MP) is the primary cause of community-acquired lung inflammation. The MP-induced manifestations of pneumonia are associated with the release of pro-inflammatory cytokines; however, the mechanisms of MP-induced inflammation have not been fully clarified. The purpose of the present study was to determine whether long noncoding RNA HOXA cluster anti-sense RNA 2 (lncRNA HOXA-AS2) is involved in MP-induced inflammation. A model of MP-induced cellular inflammation was established using the human BEAS-2B lung epithelial cell line and lncRNA HOXA-AS2 levels were detected using reverse transcription-quantitative (RT-q) PCR. MTT and flow cytometric analysis were used to assess cell viability and apoptosis, respectively. The secretion of pro-inflammatory factors including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were measured by ELISA, and protein levels of phosho- (p-)p65 and p-NF-κB inhibitor α (p-IκBα) were detected by western blotting. The results suggest that MP infection significantly decreases the level of lncRNA HOXA-AS2 in BEAS-2B cells. lncRNA HOXA-AS2 overexpression significantly enhanced cell viability, inhibited apoptosis, decreased pro-inflammatory factor expression (TNF-α, IL-β and IL-6) and inhibited NF-κB pathway activation in MP-stimulated BEAS-2B cells. Conversely, lncRNA HOXA-AS2-knockdown resulted in the opposite effects. In conclusion, lncRNA HOXA-AS2 is involved in MP infection-induced inflammation and regulates the NF-κB signaling pathway.