Abstract: Objective To investigate the role of miR-96-5p in the regulation of type 2 diabetes mellitus (T2DM)-associated pulmonary tuberculosis (PTB). 
Methods A T2DM-associated PTB mouse model was constructed. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to analyze the expression of miR-96-5p in lung tissue of mice with T2DM-associated PTB. Masson staining and HE staining were used to analyze pulmonary fibrosis and lung injury. The expression of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway-related proteins was detected by immunohistochemistry and Western blot. The levels of free fatty acids (FFA) and triglyceride in serum were analyzed by kits. 
Results MiR-96-5p was highly expressed in the lung tissue of mice with T2DM-associated PTB. Inhibition of miR-96-5p could reduce fibrosis and lung injury in lung tissue, reduce the levels of interleukin (IL) -6, tumor necrosis factor-α (TNF-α) and IL-1β in lung tissue and serum of mice with T2DM-related PTB, and reduce the levels of FFA and triglyceride in lung tissue of mice with T2DM-related PTB. The expression of p-JAK2 and p-STAT3 was up-regulated in the lung tissue of mice with T2DM-related PTB. JAK/STAT signaling pathway inhibitor (AZD1480) could reverse the promoting effect of miR-96-5p overexpression on pulmonary fibrosis and lung injury in T2DM-related PTB mouse model, and could weaken the promoting effect of miR-96-5p overexpression on the levels of IL-6, TNF-α and IL-1β in lung tissue and serum of mice with T2DM-related PTB, and reduce the levels of FFA and triglyceride in serum. 
Conclusion miR-96-5p promotes inflammatory responses of mice with T2DM-associated PTB by regulating the JAK/STAT signaling pathway. 

Key words: diabetes mellitus, type 2, tuberculosis, pulmonary, microRNAs ,