MicroRNA-20a promotes inflammation via the nuclear factor-B signaling pathway in pediatric pneumonia

Pneumonia is a common respiratory disease worldwide, which is preventable and treatable; however, it is recognized as a leading cause of mortality in children. The present study aimed to investigate the role and mechanism of microRNA (miR)-20a in inflammation in pediatric pneumonia. Clinical serum samples were collected from children with pneumonia and healthy children. Initially, the serum expression levels of miR-20a were detected by reverse transcription-quantitative polymerase chain reaction. Subsequently, A549 cells were randomly divided into four groups: Control group; lipopolysaccharide (LPS; 1 mu g/ml) group; LPS + miR-20a group; and LPS + miR-20a + pyrrolidine dithiocarbamate (PDTC; 100 mmol/l) group. The concentrations of interleukin-6 (IL-6), tumor necrosis factor (TNF)- and C-reactive protein (CRP) in clinical serum samples and A549 cells were determined by ELISA. In addition, the protein expression levels of inhibitor of nuclear factor (NF)-B (IB) and phosphorylated (p)-NF-B were measured by western blotting. The results demonstrated that miR-20a was upregulated in children with pneumonia and in lung cells with LPS-induced inflammatory injury (P<0.01). In addition, compared with the LPS group, cells in the LPS + miR-20a group exhibited increased expression levels of IL-6, TNF- and CRP (P<0.05). Overexpression of miR-20a also resulted in upregulation of the expression levels of IB and p-NF-B compared with in the LPS group (P<0.05). Furthermore, treatment with the NF-B inhibitor PDTC inhibited the expression of inflammatory factors compared with in the LPS + miR-20a group (P<0.05). In conclusion, the present study indicated that miR-20a is upregulated in pediatric pneumonia, and overexpression of miR-20a may promote inflammation through activation of the NF-B signaling pathway.