Molestina Robert E, Sinai Anthony P
Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Cell Microbiol. 2005 Mar;7(3):351-62. doi: 10.1111/j.1462-5822.2004.00463.x.
Toxoplasma gondii activates the NF-kappaB pathway in the infected host cell resulting in upregulation of pro-survival genes and prevention of apoptosis. Manipulation of the NF-kappaB cascade by T. gondii correlates with the localization of phosphorylated IkappaB at the parasitophorous vacuole membrane (PVM). This suggests a parasite-mediated event, involving the recruitment and activation of the host IkappaB kinase (IKK) complex, as has been observed with the related protozoan Theileria parva. In contrast to Theileria, confocal microscopy studies showed no apparent hijacking of IKKalpha, IKKbeta, or their activated phosphorylated forms at the T. gondii PVM. Remarkably, phosphorylation of IkappaBalpha at Ser 32/36 was observed at the PVM of T. gondii-infected IKKalpha-/-, IKKbeta-/- and IKKalpha/beta double-knockout (IKKalpha/beta-/-) fibroblasts, suggesting the involvement of a parasite kinase activity independent of host IKK. The presence of a putative T. gondii IkappaB kinase was examined by in vitro kinase assays using GST-IkappaBalpha constructs and protein extracts from both extracellular parasites and PVM fractions. Interestingly, an activity capable of phosphorylating IkappaBalpha at the critical Ser 32/36 sites was identified in parasite extracts, a property restricted to the IKK signalosome. Taken together, our data support the role for a T. gondii kinase involved in phosphorylation of host cell IkappaBalpha and suggest an unusual mechanism utilized by an intracellular pathogen capable of manipulating the NF-kappaB pathway.
弓形虫激活被感染宿主细胞中的核因子-κB通路,导致促生存基因上调并防止细胞凋亡。弓形虫对核因子-κB级联反应的操控与磷酸化的IκB在寄生泡膜(PVM)处的定位相关。这表明这是一个由寄生虫介导的事件,涉及宿主IκB激酶(IKK)复合物的募集和激活,正如在相关原生动物小泰勒虫中所观察到的那样。与泰勒虫不同,共聚焦显微镜研究显示在弓形虫的PVM处没有明显劫持IKKα、IKKβ或它们的激活磷酸化形式。值得注意的是,在感染弓形虫的IKKα-/-、IKKβ-/-和IKKα/β双敲除(IKKα/β-/-)成纤维细胞的PVM处观察到IκBα在Ser 32/36处的磷酸化,这表明存在一种独立于宿主IKK的寄生虫激酶活性。通过使用GST-IκBα构建体以及来自细胞外寄生虫和PVM组分的蛋白质提取物进行体外激酶测定,来检测是否存在假定的弓形虫IκB激酶。有趣的是,在寄生虫提取物中鉴定出一种能够在关键的Ser 32/36位点磷酸化IκBα的活性,这种特性仅限于IKK信号体。综上所述,我们的数据支持一种参与宿主细胞IκBα磷酸化的弓形虫激酶的作用,并表明一种细胞内病原体用于操控核因子-κB通路的不同寻常机制。