沙眼衣原體（Chlamydia trachomatis）感染為眼科最常見的細(xì)菌性疾病,。沙眼衣原體可引起沙眼,、結(jié)膜炎,、肺炎,、泌尿生殖道感染及性病淋巴肉芽腫等,。同很多其他細(xì)胞內(nèi)病原體一樣,，沙眼衣原體也依賴于宿主的類脂來生長。
日前,，德國研究人員在被感染的HeLa上皮細(xì)胞中發(fā)現(xiàn)了沙眼衣原體獲取其類脂的一個(gè)機(jī)制,。
在正常細(xì)胞中，高爾基體的作用是,，修飾新合成的蛋白和類脂,，供在細(xì)胞內(nèi)或細(xì)胞外分配,。沙眼衣原體的細(xì)胞內(nèi)復(fù)制觸發(fā)高爾基體分解，通過基質(zhì)蛋白golgin-84的解理產(chǎn)生功能完好的高爾基體小堆棧,。這些高爾基體小堆棧（它們在細(xì)菌內(nèi)含物周圍排列）似乎可提供一個(gè)渠道,，病原體通過該渠道可獲得類脂的供應(yīng)。
這項(xiàng)工作表明,，炎性“半胱天冬酶”（caspases）和“鈣激活酶”（calpains）在機(jī)制上是有所參與的,，它們也許可用作抗衣原體藥物的新穎的分子目標(biāo)。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 457, 731-735 (5 February 2009) | doi:10.1038/nature07578
Chlamydia causes fragmentation of the Golgi compartment to ensure reproduction
Dagmar Heuer1, Anette Rejman Lipinski1, Nikolaus Machuy1, Alexander Karlas1, Andrea Wehrens1, Frank Siedler3, Volker Brinkmann2 & Thomas F. Meyer1
1 Department of Molecular Biology,
2 Microscopy Core Facility, Max Planck Institute for Infection Biology, Charitéplatz 1, 10117 Berlin, Germany
3 Department of Membrane Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany
The obligate intracellular bacterium Chlamydia trachomatis survives and replicates within a membrane-bound vacuole, termed the inclusion, which intercepts host exocytic pathways to obtain nutrients1, 2, 3. Like many other intracellular pathogens, C. trachomatis has a marked requirement for host cell lipids, such as sphingolipids and cholesterol, produced in the endoplasmic reticulum and the Golgi apparatus4, 5, 6. However, the mechanisms by which intracellular pathogens acquire host cell lipids are not well understood1, 2, 3. In particular, no host cell protein responsible for transporting Golgi-derived lipids to the chlamydial inclusions has yet been identified. Here we show that Chlamydia infection in human epithelial cells induces Golgi fragmentation to generate Golgi ministacks surrounding the bacterial inclusion. Ministack formation is triggered by the proteolytic cleavage of the Golgi matrix protein golgin-84. Inhibition of golgin-84 truncation prevents Golgi fragmentation, causing a block in lipid acquisition and maturation of C. trachomatis. Golgi fragmentation by means of RNA-interference-mediated knockdown of distinct Golgi matrix proteins before infection enhances bacterial maturation. Our data functionally connect bacteria-induced golgin-84 cleavage, Golgi ministack formation, lipid acquisition and intracellular pathogen growth. We show that C. trachomatis subverts the structure and function of an entire host cell organelle for its own advantage.
