Diagnostic value of microRNA‑125b in peripheral blood mononuclear cells for pulmonary tuberculosis

Pulmonary tuberculosis (TB) is a chronic respiratory infectious disease. Certain microRNAs (miRNAs or miRs) are reported to be involved in regulating TB progression. The present study aimed to evaluate the diagnostic potential of miR‑125b in pulmonary TB. The expression levels of miR‑125b and Raf1 proto‑oncogene serine/threonine protein kinase (RAF1) were analyzed via reverse transcription‑quantitative (RT‑q)PCR in patients with TB. The correlation between miR‑125b and the clinical indicators was investigated, and a receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value of miR‑125b. The relationship between miR‑125b and RAF1 was examined using the dual luciferase reporter gene assay. IL‑6, TNF‑α, NF‑κB and IFN‑γ levels were detected using ELISA kits, and then the correlation between miR‑125b expression and the levels of IL‑6, TNF‑α, NF‑κB, IFN‑γ and RAF1 in peripheral blood mononuclear cells (PBMCs) was analyzed. Moreover, RAF1 mRNA and protein expression levels were detected via RT‑qPCR and western blotting. The results demonstrated that miR‑125b expression was decreased in patients with TB, while RAF1 expression was increased. Furthermore, miR‑125b expression was associated with sputum acid‑fast bacillus smear. The area under the ROC curve of miR‑125b was 0.9413, and the sensitivity and specificity of miR‑125b expression for TB were 90 and 92.5%, respectively. IL‑6, TNF‑α, NF‑κB and IFN‑γ levels were negatively correlated with miR‑125b expression, and were inhibited by miR‑125b in PBMCs. Moreover, miR‑125b targeted RAF1 to negatively regulate its expression levels. RAF1 reversed the role of miR‑125b in attenuating IL‑6, TNF‑α, NF‑κB and IFN‑γ levels in PBMCs. The present study demonstrated that the levels of IL‑6, TNF‑α, NF‑κB and IFN‑γ were negatively correlated with miR‑125b expression in PBMCs. Thus, it was suggested that miR‑125b served important roles in the occurrence and development of TB by decreasing the levels of IL‑6, TNF‑α, NF‑κB and IFN‑γ by inhibiting RAF1.