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Publication: Roca et al., 2022 - Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport
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Fig. 2

Fig. 2. TNF induces RET mROS at complex I in mycobacterium-infected macrophages.

(A and B) Illustrations of mROS production at complex I during forward electron transport (A) and reverse electron transport (B). FAD, flavin adenine dinucleotide; ΔΨ, membrane potential; IMM, inner mitochondrial membrane; ADP/ATP, adenosine diphosphate/triphosphate; cytC, cytochrome C; I to V, complexes I to V; zigzag arrows, induction; red blunted arrows, inhibition. (C to H) Quantification of mROS in larvae 1 day after infection with Mm [(C) to (E)] or Mtb [(F) to (H)] that are wild-type treated with rotenone or vehicle (C); wild-type or TNF^hi treated with rotenone or vehicle (D); wild-type, TNF^hi, or TNF^hi expressing AOX (E); wild-type or TNF^hi (F); wild-type treated with rotenone or vehicle (G); or wild-type or TNF^hi treated with rotenone or vehicle (H). Horizontal bars denote means; *P < 0.05, **P < 0.01, ****P < 0.0001 [one-way ANOVA with Dunn’s post-test in (C), (G), and (H); Tukey’s post-test in (D) and (E); uncorrected Dunn’s post-test in (F)]. Black and red symbols in (C), (F), and (G) represent uninfected (ui) and infected macrophages, respectively, in the same animals. Data are representative of two or three independent experiments [(C to G)] or a single experiment (H).

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