Clinical Diagnostic and Prognostic Evaluation of miR-136-5p in Children with Severe Pneumonia: A Case-Control and Cohort Study.

Severe pneumonia is a leading cause of childhood morbidity and mortality. MicroRNA‑136‑5p (miR‑136‑5p) plays critical roles in inflammatory diseases, yet its expression, clinical relevance, and regulatory mechanisms in children with severe pneumonia remain unclear. This study recruited 114 children with severe pneumonia and 106 healthy controls; peripheral blood miR‑136‑5p and Argonaute 1 (AGO1) were detected by quantitative real‑time polymerase chain reaction (qRT‑PCR). Receiver operating characteristic (ROC) curves, Kaplan‑Meier analysis, and multivariate Cox regression were used to evaluate diagnostic and prognostic values, whereas lipopolysaccharide (LPS)‑stimulated THP‑1 macrophages and dual‑luciferase reporter assays validated the targeting relationship between miR‑136‑5p and AGO1. Significant miR‑136‑5p upregulation was observed in patients, with favorable diagnostic efficacy (area under the curve [AUC] = 0.845). Its expression was positively correlated with white blood cell (WBC), neutrophil (NEU), procalcitonin (PCT), C‑reactive protein (CRP), brain natriuretic peptide (BNP), and D‑dimer, while negatively correlated with lymphocyte (LYM) levels. Higher miR-136-5p expression was independently associated with an increased risk of composite adverse events (hazard ratio [HR] = 4.198, P = 0.002). In vitro, miR‑136‑5p mimics enhanced LPS‑induced interleukin‑6 (IL‑6), tumor necrosis factor‑α (TNF‑α), and interleukin‑1β (IL‑1β) release and impaired cell viability, and inhibitors reversed these effects. AGO1 was confirmed as a direct target and was downregulated in patients and negatively correlated with miR‑136‑5p (r = -0.864), and AGO1 overexpression partially reversed miR‑136‑5p‑related reduced cell viability and inflammation. Collectively, miR‑136‑5p discriminates children with severe pneumonia from healthy controls. In LPS‑stimulated THP‑1‑derived macrophages, miR‑136‑5p promotes inflammation by targeting AGO1, and the miR‑136‑5p/AGO1 axis warrants further mechanistic and pre‑clinical investigation.