Clinical significance of miR-766-3p in severe pneumonia in children and its associated molecular mechanisms

Introduction: Severe pneumonia in children is a critical cause of childhood mortality. miR-766-3p is a known anti-inflammatory factor. The aim of our study is to investigate the clinical value of miR-766-3p and the molecular mechanisms by which miR-766-3p regulates severe pneumonia. Methods: The relative levels of miR-766-3p in participants' plasma were detected by quantitative real-time PCR (RT-qPCR). The diagnostic performance and prognostic value of miR-766-3p were assessed using receiver operating characteristic (ROC) curves, Kaplan–Meier (KM) curves, and Cox regression models. In vitro, lipopolysaccharide (LPS) was employed to mimic the pneumonia environment. Cell viability was tested by Cell Counting kit-8 (CCK-8) assay. The levels of inflammatory factor were measured via RT-qPCR and Enzyme-linked immunosorbent assay (ELISA). Results: The levels of miR-766-3p were diminished by 0.36-fold in children with severe pneumonia, and it effectively distinguished between children with severe pneumonia and healthy children. In pediatric patients, the accumulative survival rate was lower in low miR-766-3p expression group (average miR-766-3p level ≤ 0.65) compared to high expression group (average miR-766-3p level > 0.65 ). Multivariable Cox proportional hazards regression model analysis indicated that miR-766-3p was an independent risk factor for poor patient outcomes. Moreover, miR-766-3p mimic attenuated the inhibition of cell viability and interleukin-10 (IL-10) levels as well as the promotion of levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) caused by LPS. These effects were further abolished by Mucin 19 (MUC19) upregulation. Conclusion: miR-766-3p has potential as a diagnostic and prognostic biomarker. Mechanistically, miR-766-3p alleviates LPS-induced inflammation in MRC-5 cells by modulating MUC19.