ArticleHereditas2026
Exosomal lncRNA DLEU2 aggravates inflammatory injury and apoptosis in pediatric viral pneumonia via the miR-330-5p.
Article in Hereditas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Extracellular-Vesicle-Associated Nucleic Acids in the Diagnosis and Treatment of Respiratory Diseases: A Narrative Review.Pharmaceutics · 2026Review
- Dysregulated expression of the EMX2OS/miR-34c-5p/TBL1XR1 regulatory axis: a novel signature for severe community-acquired pneumonia in children.BMC pediatrics · 2026Article
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundViral 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. MATERIALS: 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.
resultsExosomal 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.
conclusionDLEU2 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.
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