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. 2013 Nov 18;110(49):E4790–E4797. doi: 10.1073/pnas.1320118110

Fig. 1.

Fig. 1.

Mtb with transposon-disrupted Rv0431 lacks VirR protein and is attenuated and hyperinflammatory in primary human macrophages. (A) Whole-cell lysates of WT, VirR-deficient (Tn:Rv0431), and VirR-complemented (Tn:Rv0431::Rv0431) Mtb strains were immunoblotted with antiserum against VirR. The lysates also were blotted with antiserum against hydroxyoxoadipate synthase (HOAS) as a loading control. (B and C) Human macrophages were infected with WT, VirR-deficient, or VirR-complemented Mtb at an MOI of 1, 3, and 5, and induction of TNF-α (B) and IL-6 (C) was assessed 48 h postinfection. Data points represent the mean ± SD of samples in triplicate, and results are shown from one representative experiment of two. (D) Human macrophages cultured and maintained at 10% O2 were infected with WT, VirR-deficient, or VirR-complemented Mtb at MOI 0.1, and survival was assessed. Data points represent the mean ± SD of samples in triplicate, and results are shown from one representative experiment of five. (E) Growth of VirR-deficient Mtb was compared with WT and VirR-complemented Mtb in liquid 7H9 medium at either 1% O2 (hypoxic) or 20% O2 (hyperoxic for tissue).