Let7f‑5p attenuates inflammatory injury in invitro pneumonia models by targeting MAPK6.

Abstract

Pneumonia accounts for ~1.3 million mortalities in children per year worldwide. MicroRNAs are implicated in several diseases, including cancer and pneumonia; however, the role of let7f-5p in pneumonia is not completely understood. In the present study, lipopolysaccharide (LPS) was used to establish an in vitro pneumonia model in A549 and WI-38 cells. The reverse transcription-quantitative PCR (RT-qPCR) and western blotting results demonstrated that let7f-5p expression levels were significantly decreased, whereas MAPK6 expression levels were significantly increased in the peripheral venous blood of patients with pneumonia and in LPS-induced A549 and WI-38 cells compared with healthy volunteers and control cells, respectively. Furthermore, the dual-luciferase reporter assay demonstrated that let7f-5p targeted the 3′-untranslated region of MAPK6. The ELISA and RT-qPCR results demonstrated that let7f-5p mimic ameliorated LPS-induced inflammatory injury in A549 and WI-38 cells, as demonstrated by decreased expression levels of proinflammatory cytokines, including TNF-α and IL-6. In addition, the Cell Counting Kit-8 assay results indicated that let7f-5p mimic ameliorated LPS-induced reductions in cell viability, and the western blotting results demonstrated that let7f-5p mimic reversed LPS-induced activation of the STAT3 signaling pathway. Notably, the aforementioned let7f-5p-mediated effects were reversed by MAPK6 overexpression. Collectively, the results of the present study suggested that let7f-5p inhibited inflammation by targeting MAPK6 in the in vitro pneumonia model, thus let7f-5p may serve as a potential novel therapeutic target for pneumonia.