The potential of microRNA-1180-3p as a biomarker for severe childhood pneumonia and its targeting of KANSL1

Severe pneumonia in children is a serious threat to life and health, and there is an urgent need to explore efficient biomarkers. MicroRNA-1180-3p (miR-1180-3p) has been reported to be upregulated in community-acquired pneumonia and is involved in inflammatory and immune regulation. Therefore, this study selected this molecule to investigate its diagnostic value and underlying mechanism. The study consisted of clinical investigations and in vitro mechanistic studies. In the clinical part, the study included 83 children with mild pneumonia and 53 children with severe pneumonia. The expression level of miR-1180-3p in serum was detected by quantitative real-time PCR (RT-qPCR). The diagnostic efficacy and associated factors were analyzed using receiver operating characteristic (ROC) curves and logistic regression analysis. In the mechanistic part, the regulation of cell viability and inflammatory factors (TNF-α, IL-6, and IL-1β) was verified using a lipopolysaccharide (LPS) induced A549 cell model. The target gene, KANSL1 , was verified using a luciferase reporter assay. The serum expression of miR-1180-3p in the severe pneumonia group was significantly increased, with an area under the ROC curve (AUC) of 0.862, a sensitivity of 75.47%, and a specificity of 84.34%. Multivariable logistic regression analysis revealed that miR-1180-3p ( OR = 4.323, 95% CI : 1.594–11.729) was independently associated with severe pneumonia, with a positive correlation observed with inflammatory markers such as white blood cell (WBC), neutrophils, procalcitonin (PCT), and C-reactive protein (CRP). In cellular models, inhibiting miR-1180-3p reversed the decrease in cell viability and elevation of inflammatory factors induced by LPS, and these effects were partially mediated through the downregulation of KANSL1 . This study demonstrated that miR-1180-3p represents a promising candidate biomarker for severe pneumonia in children; however, validation in larger prospective cohorts is required. In vitro experiments suggest that miR-1180-3p may modulate inflammatory responses through KANSL1 in LPS-induced cell model. Further research is needed to elucidate the downstream signaling pathways involved and to confirm the in vivo relevance of these findings.