MiR‐545‐3p: A Potential Diagnostic and Prognostic Biomarker for NRDS and Regulator of Inflammation via TNFSF13B

BACKGROUND: Neonatal respiratory distress syndrome (NRDS) is a severe respiratory disease prevalent in preterm neonates. Pulmonary inflammation is an important factor that exacerbates disease severity and prolongs the clinical course of NRDS. AIM: This study investigated the potential diagnostic and prognostic value of miR-545-3p in NRDS and its regulatory effect on cell inflammation by targeting TNFSF13B, providing a preliminary experimental basis for NRDS research. METHODS: A total of 300 preterm neonates were enrolled, including 150 with NRDS and 150 non-NRDS controls. MiR-545-3p and TNFSF13B expression in plasma was detected by RT-qPCR. The targeting relationship between miR-545-3p and TNFSF13B was validated using bioinformatics analysis and a dual-luciferase reporter assay. LPS-treated A549 cells served as an inflammatory epithelial injury model, with cell viability and inflammatory factor levels assessed by CCK-8 and ELISA assays, respectively. RESULTS: MiR-545-3p exhibited significant downregulation in neonates with NRDS, and its close correlation with LUS and SNAPPE-II scores suggests diagnostic and prognostic potential. ROC and logistic analyses evaluated its diagnostic value (AUC = 0.748; OR = 0.139, 95% CI: 0.083-0.233, p < 0.001) and prognostic value for non-survival (AUC = 0.792; OR = 0.173, 95% CI: 0.067-0.446, p < 0.001). TNFSF13B was identified as the direct target. The inhibitory effects of miR-545-3p on LPS-induced reduction of A549 cell viability and pro-inflammatory factor secretion were reversed by TNFSF13B overexpression. CONCLUSIONS: MiR-545-3p may serve as a potential auxiliary molecular marker for the diagnosis and prognostic evaluation of NRDS. The miR-545-3p/TNFSF13B axis may be involved in regulating pulmonary inflammation in NRDS.