miR-19a-3p as a biomarker for distinguishing severe pneumonia in children by targeting MXD1

Severe pneumonia (SP) contributes substantially to childhood morbidity and mortality worldwide. We assessed circulating miR-19a-3p as a biomarker for distinguishing severe from non-severe pneumonia in children and investigated its downstream target MXD1. miR-19a-3p levels were quantified via RT-qPCR in 96 pneumonia and 108 SP patients. The effects of miR-19a-3p knockdown on cell viability, inflammatory cytokines, and oxidative stress were assessed in LPS-stimulated BEAS-2B cells. Dual-luciferase assay confirmed miR-19a-3p binding to MXD1. Co-transfection with si-MXD1 tested whether MXD1 mediated the protective effects of miR-19a-3p inhibition. miR-19a-3p was higher in SP cases, with an ROC AUC of 0.894. Multivariate regression showed miR-19a-3p and D-dimer as independent risk factors. In LPS-stimulated BEAS-2B cells, blocking miR-19a-3p alleviated inflammatory responses, reduced MDA content, raised SOD activity, and improved cell viability. Luciferase assays validated MXD1 as a direct target of miR-19a-3p. MXD1 expression correlated negatively with miR-19a-3p in patient samples ( r = -0.685). Knocking down MXD1 partially offset the effects of miR-19a-3p inhibition, indicating that miR-19a-3p acts largely through MXD1 suppression. miR-19a-3p was upregulated in children with SP and exhibited strong ability to discriminate severe from non‑severe pneumonia, suggesting its value as a non‑invasive biomarker for discriminating disease severity. In airway epithelial cells, miR-19a-3p drove inflammatory responses and oxidative injury through suppression of MXD1, raising the possibility of targeting this axis therapeutically. Not applicable.