Exosomal lncRNA DLEU2 aggravates inflammatory injury and apoptosis in pediatric viral pneumonia via the miR-330-5p

Viral pneumonia (VP) is a major cause of severe respiratory illness in children. lncRNAs are involved in disease progression by regulating immune regulation. This study investigates the clinical value and regulatory function of exosomal DLEU2 in pediatric VP. Include 247 pediatric VP cases, divided into 120 mild and 127 severe groups, and collected plasma exosomes samples. The abundance of DLEU2, miR-330-5p, and CEBPD were quantified using qRT-PCR. ROC curves and logistic regression were performed to determine the diagnostic and prognostic utility. The correlation was assessed between DLEU2 level and clinical indicators. A VP cell model was established by stimulating BEAS-2B with Poly(I: C). Cell transfection, ELISA, flow cytometry and dual-luciferase reporter assays were conducted to detect cytokines, apoptosis level and target gene regulation. Exosomal DLEU2 was elevated in severe VP and showed good diagnostic performance in distinguishing severe from mild disease. High DLEU2 was independently associated with increased disease severity and correlated with adverse status, including tachypnea, respiratory retractions, reduced SpO2, and elevated inflammatory markers. Poly(I: C) stimulation upregulated DLEU2 and promoted cytokine IL-6 and IL-8 secretion and apoptosis in BEAS-2B. Silencing DLEU2 markedly attenuated these effects. DLEU2 functioned as a ceRNA by sponging miR-330-5p, thereby relieving its inhibitory effect on CEBPD. Restoration of miR-330-5p reversed DLEU2-mediated inflammatory and apoptotic responses. DLEU2 is upregulated in pediatric VP and is associated with disease severity. Functional assays suggest that DLEU2 may aggravate inflammatory injury in bronchial epithelial cells via miR-330-5p.