Downregulation of miR-409-3p suppresses LPS-induced inflammation in human bronchial epithelial cells through SOCS3/JAK1/STAT3 signaling: The implication for bronchopneumonia

Abstract

In recent decades, the role of microRNAs (miRs) in the development of pneumonia has been reported by a number of researchers. The present study aimed to investigate the role of miR-409-3p in lipopolysaccharide (LPS)-induced human bronchial epithelial cells and the implication for bronchopneumonia. An in vitro inflammation model was established using LPS-induced BEAS-2B cells. Cell apoptosis was determined by flow cytometry. Inflammatory factors were detected by ELISA and reverse transcription-quantitative PCR. Protein levels of Janus kinase 1 (JAK1)/STAT3 and suppressor of cytokine signaling (SOCS)3 were determined by western blotting. Dual-luciferase reporter assay was performed to confirm the interaction between miR-409-3p and SOCS3. LPS treatment significantly increased miR-409-3p expression and decreased the expression levels of SOCS3 in BEAS-2B cells. Dual-luciferase reporter assay demonstrated that miR-409-3p directly targeted and negatively regulated SOCS3. Inhibition of miR-409-3p markedly decreased the levels of TNF-α, IL-6 and IL-1β, and suppressed apoptosis induced by LPS, which was reversed by SOCS3-knockdown. The inhibition of SOCS3 significantly activated JAK1/STAT3 signaling, as well as enhancing the levels of TNF-α, IL-6 and IL-1β, and promoting apoptosis, which was reversed by the JAK1 inhibitor Tofacitinib. Suppression of miR-409-3p improved LPS-induced inflammation through SOCS3 in LPS-treated BEAS-2B cells, and this may be caused by regulating JAK1/STAT3 signaling.