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

Background: 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. Methods: 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. Results: 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. Conclusion: miR-224-5p may hold diagnostic potential in NP miR-224-5p may regulate inflammatory responses in NP by targeting PTX3.