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Editorial
. 2022 Jun;14(6):1758-1765.
doi: 10.21037/jtd-22-39.

The potential role for metformin in the prevention and treatment of tuberculosis

Alex Sutter  1 , Dylan Landis  1 , Kenneth Nugent  1
Affiliations
Editorial

The potential role for metformin in the prevention and treatment of tuberculosis

Alex Sutter et al. J Thorac Dis. 2022 Jun.
No abstract available

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Conflict of interest statement

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-22-39/coif). The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Summary of metformin’s host-directed immunomodulatory effects. Metformin decreases production of MPPs and systemic monocyte activation markers, including sCD14, sCD163, sTF, and CRP (24,25). A reduction of inflammatory mediators, including TNF-α, IL-1β, IL-6, IFN-γ, and IL-17, also contributes to metformin’s ability to limit lung tissue destruction, decrease bacillary numbers, and reduce cavity formation (23,26). Furthermore, metformin augments host cell immune responses by enhancing phagocytosis and increasing mitochondrial ROS production (12,26). Through these host-directed therapeutic effects, metformin could improve intracellular killing of tuberculosis bacilli and limit the development of tuberculous infection and disease. sCD14, soluble cluster of differentiation; sCD163, soluble CD163; sTF, soluble tissue factor; CRP, C-reactive protein; TNF-α, tumor necrosis factor-alpha; IL, interleukin; IFN-γ, interferon-gamma; ROS, reactive oxygen species; MPPs, matrix metalloproteases.
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References

    1. World Health Organization. Global tuberculosis report 2021. WHO 2021. Available online: https://www.who.int/teams/global-tuberculosis-programme/tb-reports/globa...
    1. Yew WW, Chang KC, Chan DP, et al. Metformin as a host-directed therapeutic in tuberculosis: Is there a promise? Tuberculosis (Edinb) 2019;115:76-80. 10.1016/j.tube.2019.02.004 - DOI - PubMed
    1. Ryndak MB, Laal S. Mycobacterium tuberculosis Primary Infection and Dissemination: A Critical Role for Alveolar Epithelial Cells. Front Cell Infect Microbiol 2019;9:299. 10.3389/fcimb.2019.00299 - DOI - PMC - PubMed
    1. Jeon CY, Murray MB. Diabetes mellitus increases the risk of active tuberculosis: a systematic review of 13 observational studies. PLoS Med 2008;5:e152. 10.1371/journal.pmed.0050152 - DOI - PMC - PubMed
    1. Restrepo BI, Schlesinger LS. Host-pathogen interactions in tuberculosis patients with type 2 diabetes mellitus. Tuberculosis (Edinb) 2013;93 Suppl:S10-4. 10.1016/S1472-9792(13)70004-0 - DOI - PMC - PubMed

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