{"title":"MiR-128-3p serves as a diagnostic biomarker in pediatric Mycoplasma pneumoniae pneumonia.","authors":"Hong Yang, Wanzhen Yang, Dan Li","doi":"10.1186/s12890-026-04553-z","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Mycoplasma pneumoniae pneumonia (MPP) is a frequent pulmonary infection in children, and severe cases are associated with significant adverse outcomes.</p><p><strong>Purpose: </strong>To investigate the expression, clinical value, and functional mechanism of miR-128-3p in MPP.</p><p><strong>Methods: </strong>Serum samples from children with MPP were collected to measure miR-128-3p expression. ROC curve and logistic analysis were further performed to evaluate the clinical value of miR-128-3p in MPP. An MPP model was established by infecting BEAS-2B cells with Mycoplasma pneumoniae (MP). The functions of miR-128-3p were verified using CCK-8 and ELISA. Potential downstream target genes were predicted and verified by bioinformatics analysis and the dual-luciferase reporter assay.</p><p><strong>Results: </strong>MiR-128-3p was significantly downregulated in the serum of children with MPP and served as an independent predictor of severe MPP (SMPP). Overexpression of miR-128-3p inhibited the secretion of IL-6, IL-8, and TNF-α and alleviated cell injury. ITGA5 is a target gene of miR-128-3p, which was upregulated in MPP. Rescue experiments verified that overexpression of ITGA5 abolished the anti‑inflammatory and protective effects of miR‑128‑3p.</p><p><strong>Conclusion: </strong>MiR-128-3p is downregulated in MPP and serves as a predictive biomarker for SMPP, which exerts a protective effect by suppressing inflammatory responses.</p>","PeriodicalId":9148,"journal":{"name":"BMC Pulmonary Medicine","volume":"26 1","pages":""},"PeriodicalIF":3.1000,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13651261/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMC Pulmonary Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12890-026-04553-z","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"RESPIRATORY SYSTEM","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Mycoplasma pneumoniae pneumonia (MPP) is a frequent pulmonary infection in children, and severe cases are associated with significant adverse outcomes.
Purpose: To investigate the expression, clinical value, and functional mechanism of miR-128-3p in MPP.
Methods: Serum samples from children with MPP were collected to measure miR-128-3p expression. ROC curve and logistic analysis were further performed to evaluate the clinical value of miR-128-3p in MPP. An MPP model was established by infecting BEAS-2B cells with Mycoplasma pneumoniae (MP). The functions of miR-128-3p were verified using CCK-8 and ELISA. Potential downstream target genes were predicted and verified by bioinformatics analysis and the dual-luciferase reporter assay.
Results: MiR-128-3p was significantly downregulated in the serum of children with MPP and served as an independent predictor of severe MPP (SMPP). Overexpression of miR-128-3p inhibited the secretion of IL-6, IL-8, and TNF-α and alleviated cell injury. ITGA5 is a target gene of miR-128-3p, which was upregulated in MPP. Rescue experiments verified that overexpression of ITGA5 abolished the anti‑inflammatory and protective effects of miR‑128‑3p.
Conclusion: MiR-128-3p is downregulated in MPP and serves as a predictive biomarker for SMPP, which exerts a protective effect by suppressing inflammatory responses.
期刊介绍:
BMC Pulmonary Medicine is an open access, peer-reviewed journal that considers articles on all aspects of the prevention, diagnosis and management of pulmonary and associated disorders, as well as related molecular genetics, pathophysiology, and epidemiology.