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. 2018 Jul 3;9:1367. doi: 10.3389/fmicb.2018.01367

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Copyright © 2018 Machado, Girardini, Viveiros and Pieroni.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic illustration of the M.tuberculosis cell membrane, including the electron transport chain (ETC), efflux pumps (EPs), and the site of action of several antituberculosis drugs. The great majority of the drugs (approved for tuberculosis, new or repurposed) target both enzymes (black lines) and the PMF (red). Blue line shows the classic protonophores disrupting the PMF and the green line indicates the efflux inhibitors that target several mycobacterial efflux pumps. By damaging the cell membrane, the lipophilic drugs will affect the activity of several membrane enzymes such as those involved in the ETC and efflux pumps responsible for the extrusion of several compounds from the cell. The inhibition of any component of the ETC reduces energy production and disrupts membrane potential. Consequently, the disruption of the PMF reduces the activity of the efflux pumps. Regarding the mode of action of the compounds see the text for details. NDH1, NADH dehydrogenase type I; NDH2, NADH dehydrogenase type II; SDH, succinate dehydrogenase; MK, menaquinone; Cyt C, cytochrome c; PMF, proton motive force; DPR, decaprenylphosphoryl-β-d-ribose 2′-epimerase; SMR, small multidrug resistance; ABC, ATP binding cassette; MFS, major facilitator superfamily; RND, resistance-nodulation and cell division.