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The Journal of Immunology, 2005, 174: 1701-1708.
Copyright © 2005 by The American Association of Immunologists

NF-{kappa}B Activation Is Not Required for Chlamydia trachomatis Inhibition of Host Epithelial Cell Apoptosis1

Yangming Xiao*, Youmin Zhong*, Heng Su*,{dagger}, Zhiguang Zhou{dagger}, Paul Chiao{ddagger} and Guangming Zhong2,*

* Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229; {dagger} Institute of Metabolism and Endocrinology, Central South University Xiangya Medical College, Hunan, China; and {ddagger} Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030

Chlamydia trachomatis, an obligate intracellular bacterial species, is known to inhibit host cell apoptosis. However, the chlamydial antiapoptotic mechanism is still not clear. Because NF-{kappa}B activation is antiapoptotic, we tested the potential role of NF-{kappa}B activation in chlamydial antiapoptotic activity in the current study. First, no obvious NF-{kappa}B activation was detected in the chlamydia-infected cells when these cells were resistant to apoptosis induced via either the intrinsic or extrinsic apoptosis pathways. Second, inhibition of NF-{kappa}B activation with pharmacologic reagents failed to block the chlamydial antiapoptotic activity. Finally, NF-{kappa}B p65 gene deletion did not prevent chlamydia from inhibiting host cell apoptosis. These observations together have demonstrated that NF-{kappa}B activation is not required for the chlamydial antiapoptotic activity.




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