The potential role for metformin in the prevention and treatment of tuberculosis
Abstract
including TNF- α , IL-1 β , 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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