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. 2016 May 31;71(12):1145–1153. doi: 10.1136/thoraxjnl-2015-207402

Figure 5.

Figure 5

Mycobacterium tuberculosis (M.tb) infection drives hypoxia-inducible factor (HIF)-1α accumulation in normoxia. (A) In A549 cells, conditioned media from Mtb-infected monocytes (CoMTb) stimulation and dimethyloxalyl glycine (DMOG) (0.25 mM) result in early HIF-1α stabilisation. Preincubating A549 cells with DMOG (0.25 mM) and subsequent stimulation with CoMTb markedly increase HIF-1α accumulation, peaking at 6 h. (B) M.tb infection increases HIF-1α accumulation and stabilisation in normoxia in primary human monocyte-derived macrophages (MDMs), peaking at 24 h. (C) Combined infection with M.tb and exposure to hypoxia cause greater HIF-1α accumulation than either stimulus alone, peaking at 4 h and persisting until 24 h. (D) Inhibition of HIF-1α by LW6 (range 50–100 µM) results in decreased matrix metalloproteinase-1 (MMP-1) secretion in M.tb-infected MDMs in hypoxia (hatched bars). **p<0.01.