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. 2008 Nov 24;205(12):2791–2801. doi: 10.1084/jem.20080767

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© 2008 Chen et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 3. — Effect of exogenous prostanoids produced by Mtb-infected Mφ on H37Rv-induced mitochondrial cationic dye release. (A) PGE₂ blocks DiOC₆(3) release from mitochondria of human Mφ infected with H37Rv (MOI 5:1; 48 h). A fluorescence-activated cell sorter diagram is shown. (B) Down-regulation of cationic dye release by increasing concentrations of PGE₂ (2–10 μM) is statistically significant at all PGE₂ concentrations (P < 0.01; n = 6). (C) Effect of 1 μM of various prostanoids on H37Rv-induced mitochondrial DiOC₆(3) release of Mφ. Only PGE₂ inhibition of cationic dye release from the mitochondria is statistically significant (*, P < 0.007; n = 3). PGF_2α has borderline activity. The concentration of LTB₄ is 0.1 μM. (D) H37Ra (MOI 5:1)-induced DiOC₆(3) release from mitochondria of WT and PGES^−/− mouse Mφ infected in the absence and presence of 1 μM PGE₂. At 48 h, cationic dye release from the mitochondria was measured (*, P < 0.006; n = 5). (E) 1 μM PGE₂ does not alter H37Ra- and H37Rv-induced cytochrome c release from the mitochondria (not significant; n = 3). Data are presented as means ± SE. In all studies, n represents the number of independent experiments.