Long non-coding RNA THRIL aggravates inflammatory injury in pediatric Mycoplasma pneumoniae pneumonia via sponging miR-495-3p

This study aimed to determine the expression levels of the long non-coding RNA THRIL (lncRNA THRIL) in children with Mycoplasma pneumoniae pneumonia (MPP) and evaluate its clinical significance, as well as to validate the molecular mechanism by which THRIL regulates inflammation in MPP through targeting microRNA-495-3p (miR-495-3p). The expression levels of serum THRIL and miR-495-3p were measured, and inflammatory cytokine levels were assessed. Logistic regression analysis was conducted to identify risk factors for refractory MPP (RMPP). An in vitro model of MPP cells was established, and rescue experiments were performed. A dual-luciferase reporter assay was employed to validate the target association between THRIL and miR-495-3p. Serum THRIL expression was significantly elevated in children diagnosed with MPP, particularly within the RMPP subgroup ( P < 0.001). THRIL levels exhibited a positive correlation with various inflammatory factors. Furthermore, THRIL was identified as an independent risk indicator for RMPP ( P = 0.002). THRIL directly targets and binds to miR-495-3p. In A549 cells infected with MP, THRIL knockdown significantly enhanced cellular proliferation, suppressed apoptosis, and decreased the secretion of inflammatory factors ( P < 0.01). Conversely, the under-expression of miR-495-3p partially abolished the protective effect of silencing THRIL expression in the MPP cell model. LncRNA THRIL exacerbates the inflammatory response and disease progression of MPP by regulating miR-495-3p and may function as a potential indicator for the detection and treatment for RMPP in children. Not applicable.