Lei Zhang1, Lili Dong1, Yu Tang1, Min Li1, Mingming Zhang2. 1. Department of Respiration, Children's Hospital Affiliated to Zhengzhou University (Zhengzhou Children's Hospital), Zhengzhou City, China. 2. Department of Pediatrics, Zaozhuang Municipal Hospital, Zaozhuang City, China.
Abstract
Background: Pneumonia is a common respiratory disease worldwide that can be prevented and treated. However, it is considered to be the leading cause of children death. The present study was aimed to explore the functional role and molecular mechanism of miR-146b in the inflammation injury in pediatric pneumonia.Materials and methods: The lipopolysaccharide (LPS)-induced pulmonary injury cell model was established in WI-38 human lung fibroblasts cells. QRT-PCR and Western blot was applied to detect miR-146b and MyD88 expression. ELISA assay was used to analyze the production of pro-inflammatory factors. Cell viability was evaluated by CCK-8 assay. The apoptosis proteins and the downstream genes of NF-κB pathway were detected by Western blot. Results: we displayed that miR-146b was down-regulated, whereas MyD88 was up-regulated in the serum of children patients with pneumonia and in WI-38 cells treated with LPS. Moreover, re-expression of miR-146b suppressed the production of inflammatory factors in the serum of pneumonia patients and WI-38 cells treated with LPS. In addition, elevating miR-146b expression increased WI-38 cell viability and reduced cell apoptosis. More importantly, bioinformatics analysis revealed that MyD88 was a target of miR-146b and could overturn the protective effect of miR-146b on the inflammation injury in LPS-injured WI-38 cells. Furthermore, miR-146b over-expression inhibited the activation of NF-κB signaling pathway by suppressing MyD88. Conclusion: miR-146b attenuated the inflammation injury in pediatric pneumonia through inhibiting MyD88/NF-κB signaling pathway. These preliminarily findings further deepened our understanding of this mechanism and identified new potential therapeutic targets for pediatric pneumonia.
Background: Pneumonia is a common respiratory disease worldwide that can be prevented and treated. However, it is considered to be the leading cause of childrendeath. The present study was aimed to explore the functional role and molecular mechanism of miR-146b in the inflammation injury in pediatric pneumonia.Materials and methods: The lipopolysaccharide (LPS)-induced pulmonary injury cell model was established in WI-38human lung fibroblasts cells. QRT-PCR and Western blot was applied to detect miR-146b and MyD88 expression. ELISA assay was used to analyze the production of pro-inflammatory factors. Cell viability was evaluated by CCK-8 assay. The apoptosis proteins and the downstream genes of NF-κB pathway were detected by Western blot. Results: we displayed that miR-146b was down-regulated, whereas MyD88 was up-regulated in the serum of childrenpatients with pneumonia and in WI-38 cells treated with LPS. Moreover, re-expression of miR-146b suppressed the production of inflammatory factors in the serum of pneumoniapatients and WI-38 cells treated with LPS. In addition, elevating miR-146b expression increased WI-38 cell viability and reduced cell apoptosis. More importantly, bioinformatics analysis revealed that MyD88 was a target of miR-146b and could overturn the protective effect of miR-146b on the inflammation injury in LPS-injured WI-38 cells. Furthermore, miR-146b over-expression inhibited the activation of NF-κB signaling pathway by suppressing MyD88. Conclusion:miR-146b attenuated the inflammation injury in pediatric pneumonia through inhibiting MyD88/NF-κB signaling pathway. These preliminarily findings further deepened our understanding of this mechanism and identified new potential therapeutic targets for pediatric pneumonia.