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Trial registration UMIN000011118 (date of registration: July 4, 2013)

Establishment of comprehensive mechanistic models that incorporate mitochondrial oxidative stress, lipid metabolic reprogramming, and inflammatory amplification, to enable pathway-synergistic targeting

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Depletion of GSH (by BSO or diethylmaleate) also inhibits macrophage leishmanicidal activity, as well as NO production, while the GSH precursor GSH-ethyl ester restores them, 79 suggesting that the requirement for the GSH/NO pathway might be a common feature of resistance to intracellular pathogens

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