Inhibition of mir-224-5p by Targeting PTX3 Promotes Inflammatory Damage in Neonatal Pneumonia.

Authors

Dongqing Zhang, Huiqin Niu

Published in

International archives of allergy and immunology. Pages 1-20. Jul 22, 2026. Epub Jul 22, 2026.

Abstract

Neonatal pneumonia (NP) is one of the most serious infections affecting newborns. This study primarily investigates the diagnostic value and molecular mechanisms of miR-224-5p in NP.
A total of 165 newborns were included, comprising 85 newborns with NP and 80 healthy newborns. miR-224-5p level was detected by RT-qPCR. miR-224-5p was overexpressed or inhibited in the WI38 cells treated with LPS by cell transfection. The target of miR-224-5p was predicted through bioinformatics analysis and validated by dual luciferase assays. Cell viability and apoptosis were assessed utilizing CCK-8 assays and flow cytometry. Inflammatory cytokine levels were measured by ELISA.
In NP, plasma miR-224-5p was downregulated and had significant diagnostic value (AUC = 0.877). miR-224-5p level was closely correlated with clinical indicators of NP. In the NP model, miR-224-5p increased cell viability, inhibited apoptosis, and alleviated inflammatory responses. PTX3 may be a downstream target of miR-224-5p. PTX3 may partially reverse the attenuation of inflammatory responses caused by miR-224-5p in NP.
miR-224-5p may hold diagnostic potential in NP miR-224-5p may regulate inflammatory responses in NP by targeting PTX3.

PMID:
42485278
Bibliographic data and abstract were imported from PubMed on 23 Jul 2026.

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