• Tao Liu, Yaguo Wang, Jing Gui, Yu Fu, Chunli Ye, Xiangya Hong, Ling Chen, Yuhua Li, Xilin Zhang, and Wenxu Hong.
• Shenzhen Center for Chronic Disease Control and Prevention, Shenzhen, China.
• Medicine (Baltimore). 2022 Dec 30; 101 (52): e31652e31652.

BackgroundDiabetes mellitus patients with pulmonary tuberculosis (DMTB) comorbidity has been recognized as a major obstacle towards achieving the World Health Organization goal of reducing the tuberculosis incidence rate by 90% in 2035. Host immune responses affected by diabetes can lead to increased susceptibility, severity and poor treatment outcomes in DMTB patients, and the underlying mechanisms have not yet been fully elucidated. This study aimed to identify key immunological and cellular components that contribute to increased morbidity and mortality in DMTB cases.MethodsWe performed RNA-Seq of total RNA isolated from peripheral blood mononuclear cells from 3 TB, 3 diabetes mellitus, and 3 DMTB patients and healthy controls, and analyzed differential expression, pathway enrichment and clustering of differentially-expressed genes (DEGs) to identify biological pathways altered specifically in DMTB patients.ResultsBioinformatic analysis of DEGs suggested that enhanced inflammatory responses, small GTPases, the protein kinase C signaling pathway, hemostasis and the cell cycle pathway are likely implicated in the pathogenesis of the DMTB comorbidity.ConclusionThe DMTB comorbidity is associated with an altered transcriptome and changes in various biological pathways. Our study provides new insights on the pathological mechanism that may aid the development of host-directed therapies for this increasingly prevalent disease in high TB burden countries.Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

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