Diabetes has been associated with an increased risk of developing tuberculosis. The reasons related to the increased susceptibility to develop TB in type 2 diabetes mellitus (T2DM) individuals, has not been completely elucidated. However, this susceptibility has been attributed to several factors including failures and misfunctioning of the immune system. In the present study, we aimed to determine the role of anti-hyperglycemic drugs such as glyburide, insulin, and metformin to promote the killing of mycobacteria through the regulation of innate immune molecules such as host defense peptides (HDP) in lung epithelial cells and macrophages. Our results showed that metformin reduces bacillary loads in macrophages and lung epithelial cells which correlates with higher production of β-defensin-2, -3 and -4. Since β-defensins are crucial molecules for controlling Mycobacteriumtuberculosis growth, the present results suggest that the use of metformin would be the first choice in the treatment for T2DM2, in patients within tuberculosis-endemic areas.

中文翻译：

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二甲双胍可促进结核分枝杆菌的杀伤，并增加肺上皮细胞和巨噬细胞中人β-防御素的产生。

糖尿病与患结核病的风险增加有关。与2型糖尿病（T2DM）个体患结核病的易感性增加相关的原因尚未完全阐明。然而，这种敏感性归因于几个因素，包括免疫系统的衰竭和功能失调。在本研究中，我们旨在确定抗降糖药（如格列本脲，胰岛素和二甲双胍）通过调节先天性免疫分子（如宿主上皮细胞中的宿主防御肽（HDP））来促进分枝杆菌的杀伤作用。巨噬细胞。我们的研究结果表明，二甲双胍可降低巨噬细胞和肺上皮细胞的细菌负荷，这与β-防御素-2，-3和-4的更高产量相关。