Effect of Metformin on systemic chemokine responses during anti-tuberculosis chemotherapy

IF 2.8 3区医学 Q3 IMMUNOLOGY

Tuberculosis Pub Date : 2024-06-01 DOI:10.1016/j.tube.2024.102523

Nathella Pavan Kumar , Chandrasekaran Padmapriyadarsini , Arul Nancy , M. Tamizhselvan , Anant Mohan , Devarajulu Reddy , N. Poorana Ganga Devi , Prabakaran Rathinam , Bharathi Jeyadeepa , R.K. Shandil , Randeep Guleria , Manjula Singh , Subash Babu

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引用次数: 0

Abstract

Background

Metformin (MET), by boosting immunity, has been suggested as a host-adjunctive therapy to anti-tuberculosis treatment (ATT).

Methods

We evaluated whether adding MET to the standard ATT can alter the host chemokine response. We investigated the influence of metformin on the plasma levels of a wide panel of chemokines in a group of active tuberculosis patients before treatment, at 2nd month of ATT and at 6-months of ATT as part of our clinical study to examine the effect of metformin on ATT.

Results

Our results demonstrated that addition of metformin resulted in diminished CC (CCL1 and CCL3) and CXC (CXCL-2 and CXCL-10) chemokines in MET arm as compared to non-MET arm at the 2nd month and 6th month of ATT. In addition to this, MET arm showed significantly diminished chemokines in individuals with high bacterial burden and cavitary disease.

Conclusion

Our current data suggest that metformin alters chemokines responses that could potentially curb excessive inflammation during ATT.

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二甲双胍对抗结核化疗期间全身趋化因子反应的影响

背景二甲双胍（MET）通过增强免疫力被认为是抗结核治疗（ATT）的宿主辅助疗法。作为临床研究的一部分，我们调查了二甲双胍对一组活动性肺结核患者治疗前、ATT 第 2 个月和 ATT 第 6 个月时血浆中多种趋化因子水平的影响，以研究二甲双胍对 ATT 的影响。结果我们的研究结果表明，在 ATT 第 2 个月和第 6 个月时，与非二甲双胍治疗组相比，二甲双胍治疗组的 CC（CCL1 和 CCL3）和 CXC（CXCL-2 和 CXCL-10）趋化因子水平降低。结论：我们目前的数据表明，二甲双胍可改变趋化因子反应，从而有可能抑制 ATT 期间的过度炎症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Tuberculosis 医学-呼吸系统

CiteScore

4.60

自引率

3.10%

发文量

审稿时长

49 days

期刊介绍： Tuberculosis is a speciality journal focusing on basic experimental research on tuberculosis, notably on bacteriological, immunological and pathogenesis aspects of the disease. The journal publishes original research and reviews on the host response and immunology of tuberculosis and the molecular biology, genetics and physiology of the organism, however discourages submissions with a meta-analytical focus (for example, articles based on searches of published articles in public electronic databases, especially where there is lack of evidence of the personal involvement of authors in the generation of such material). We do not publish Clinical Case-Studies. Areas on which submissions are welcomed include: -Clinical TrialsDiagnostics- Antimicrobial resistance- Immunology- Leprosy- Microbiology, including microbial physiology- Molecular epidemiology- Non-tuberculous Mycobacteria- Pathogenesis- Pathology- Vaccine development. This Journal does not accept case-reports. The resurgence of interest in tuberculosis has accelerated the pace of relevant research and Tuberculosis has grown with it, as the only journal dedicated to experimental biomedical research in tuberculosis.