recruitment of bad by the chlamydia trachomatis vacuole correlates with host-cell survival招聘坏的沙眼衣原体液泡与宿主细胞的生存.pdfVIP

Recruitment of BAD by the Chlamydia trachomatis Vacuole Correlates with Host-Cell Survival 1 1 2 1 ¨ 2 3 1,4* Philippe Verbeke , Lynn Welter-Stahl , Songmin Ying , Jon Hansen , Georg Hacker , Toni Darville , David M. Ojcius ´ ¨ ¨ 1 Institut Jacques Monod, Universite Paris—Denis Diderot, Paris, France, 2 Institute for Medical Microbiology, Technische Universitat Munchen, Munich, Germany, 3 Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America, 4 School of Natural Sciences, University of California Merced, Merced, California, United States of America Chlamydiae replicate intracellularly in a vacuole called an inclusion. Chlamydial-infected host cells are protected from mitochondrion-dependent apoptosis, partly due to degradation of BH3-only proteins. The host-cell adapter protein 14- 3-3b can interact with host-cell apoptotic signaling pathways in a phosphorylation-dependent manner. In Chlamydia trachomatis-infected cells, 14-3-3b co-localizes to the inclusion via direct interaction with a C. trachomatis-encoded inclusion membrane protein. We therefore explored the possibility that the phosphatidylinositol-3 kinase (PI3K) pathway may contribute to resistance of infected cells to apoptosis. We found that inhibition of PI3K renders C. trachomatis-infected cells sensitive to staurosporine-induced apoptosis, which is accompanied by mitochondrial cytochrome c release. 14-3-3b does not associate with the Chlamydia pneumoniae inclusion, and inhibition of PI3K does not affect protection