Evidence map›Paper›PMID 41975260›Full record

ArticleBMC immunology2026

Study on the value and mechanism of miR-369-5p in childhood pneumonia.

Guoxia Luo, Congpo Deng, Bo Wen

Abstract read
In one paragraph

Article in BMC immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Guoxia Luo *Department of Laboratory Medicine, Chongqing University Fuling Hospital, Chongqing, 408000, China.
Congpo Deng *Department of Laboratory Medicine, The People's Hospital of kaizhou District, Chongqing, 405400, China.
Bo WenDepartment of Laboratory Medicine, Chongqing Wanzhou District Maternal and Child Health Hospital, No.8 Wanquan Road, Wanzhou District, Chongqing, 404000, China. Wenbocq@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChildhood pneumonia (CP) represents a leading cause of pediatric mortality globally. Consequently, prompt diagnosis of CP is of great significance for its treatment and prognosis.

objectiveThe objective of this study is to investigate the clinical significance of miR-369-5p in CP and its underlying mechanism.

methodsThis study enrolled clinical data from 69 CP patients and 60 healthy individuals. Through binary logistic analysis, ROC analysis, and Kaplan-Meier (KM) analysis, the diagnostic and prognostic utility of miR-369-5p for CP was determined. The RT-qPCR experiment was used to detect the expression levels of miR-369-5p, polymeric immunoglobulin receptor (PIGR), and inflammatory cytokines. The study used LPS (Lipopolysaccharide) to induce WI-38 cells to establish a pneumonia cell model for in vitro cell experiments and used the kit to detect the oxidative stress indicators. The cell proliferation and apoptosis were detected through CCK8 (Cell Counting Kit-8) and flow cytometry assays. The target genes of miR-369-5p were predicted using TargetScan database and subsequently validated via dual luciferase reporter assays. Pearson analysis revealed the correlation between miR-369-5p and PIGR.

resultsMiR-369-5p was markedly overexpressed in CP, serving as a diagnostic biomarker for CP, as well as being associated with a poor prognosis. LPS induction in WI-38 cells triggered miR-369-5p upregulation, which coincided with enhanced levels of inflammation, oxidative stress indicators and apoptosis, and a decline in proliferation capacity. PIGR was confirmed as a downstream target of miR-369-5p. Silencing miR-369-5p could lead to increased expression of PIGR, decreased expression of inflammatory factors and oxidative stress indicators, and enhanced cell activity. Meanwhile, inhibition of PIGR could weaken the effect of inhibiting miR-369-5p.

conclusionUpregulated serum miR-369-5p serves as a promising non-invasive biomarker for the diagnosis and prognosis of CP. Inhibiting miR-369-5p can ameliorates the condition of CP by targeting PIGR.

Indexed as

MicroRNAsPneumoniaApoptosisBiomarkersCell LineCell ProliferationChildChild, PreschoolCytokinesFemaleGene Expression RegulationHumansInfantLipopolysaccharidesMaleOxidative StressBiomarkersCytokinesLipopolysaccharidesMicroRNAsChildhood pneumoniaMiR-369-5pPIGR

Identifiers

PMID41975260
PMCPMC13270802

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.