Severe pneumonia (SP) is a critical infectious disease characterized by excessive inflammatory responses, and the molecular mechanisms underlying its progression remain incompletely understood. To investigate the expression pattern, diagnostic value, and potential functional regulatory mechanisms of miR-200b in SP. RT-qPCR was used to detect miR-200b expression levels; ROC curve analysis was used to evaluate its diagnostic performance; prognostic indicators of miR-200b were compared between high- and low-expression groups, and Cox regression was employed to identify independent prognostic factors. In vitro validation of the pro-inflammatory effects of miR-200b. Target genes were identified through Venn diagram-based prediction and dual luciferase reporter assays. Functional recovery experiments were conducted to elucidate regulatory pathways. miR-200b expression was significantly higher in SP patients than in CP/HC groups, with an ROC curve AUC of 0.848 distinguishing SP from CP/HC, demonstrating good diagnostic performance. Elevated miR-200b expression significantly correlated with poorer prognostic indicators and served as an independent risk factor for adverse SP outcomes. In vitro experiments demonstrated that miR-200b expression was upregulated in a concentration- and time-dependent manner following LPS stimulation, promoting IL-6 and TNF-α secretion. RHOA was identified as a direct target gene of miR-200b, and miR-200b exerts pro-inflammatory effects by inhibiting RHOA and activating the NF-κB pathway. miR-200b serves as a potential diagnostic and prognostic biomarker for SP. By targeting RHOA to activate the NF-κB pathway, it promotes inflammatory damage in SP, thus providing a novel therapeutic target for clinical intervention.
Zheng et al. (Wed,) studied this question.