Nature：沙眼衣原体获取类脂机制

沙眼衣原体（Chlamydia trachomatis）感染为眼科最常见的细菌性疾病。沙眼衣原体可引起沙眼、结膜炎、肺炎、泌尿生殖道感染及性病淋巴肉芽肿等。同很多其他细胞内病原体一样，沙眼衣原体也依赖于宿主的类脂来生长。
日前，德国研究人员在被感染的HeLa上皮细胞中发现了沙眼衣原体获取其类脂的一个机制。
在正常细胞中，高尔基体的作用是，修饰新合成的蛋白和类脂，供在细胞内或细胞外分配。沙眼衣原体的细胞内复制触发高尔基体分解，通过基质蛋白golgin-84的解理产生功能完好的高尔基体小堆栈。这些高尔基体小堆栈（它们在细菌内含物周围排列）似乎可提供一个渠道，病原体通过该渠道可获得类脂的供应。
这项工作表明，炎性“半胱天冬酶”（caspases）和“钙激活酶”（calpains）在机制上是有所参与的，它们也许可用作抗衣原体药物的新颖的分子目标。（生物谷Bioon.com）
生物谷推荐原始出处：
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, Germany3 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.