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NF-kappa B activation is not required for Chlamydia trachomatis inhibition of host epithelial cell apoptosis.

Journal of immunology (Baltimore, Md. : 1950) (2005-01-22)
Yangming Xiao, Youmin Zhong, Heng Su, Zhiguang Zhou, Paul Chiao, Guangming Zhong
RESUMEN

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-kappaB activation is antiapoptotic, we tested the potential role of NF-kappaB activation in chlamydial antiapoptotic activity in the current study. First, no obvious NF-kappaB 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-kappaB activation with pharmacologic reagents failed to block the chlamydial antiapoptotic activity. Finally, NF-kappaB p65 gene deletion did not prevent chlamydia from inhibiting host cell apoptosis. These observations together have demonstrated that NF-kappaB activation is not required for the chlamydial antiapoptotic activity.

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Parthenolide, Tanacetum parthenium, A cell-permeable sesquiterpene lactone with anti-inflammatory, antisecretory, and spasmolytic properties.