磷脂酰肌醇类脂质在嗜肺军团菌发病机制中作用的研究进展

Research progress in the role of phosphatidylinositol lipids in Legionella pneumophila pathogenesis

摘要:

嗜肺军团菌(Legionella pneumophila)是一种能引起被称为“军团病”的严重肺炎的致病菌，其利用自身的IVB型分泌系统(type IVB secretion systems)将效应蛋白转运到宿主细胞中，作用于宿主蛋白质和脂质，以形成军团菌在宿主细胞内生长所需的吞噬泡(Legionella-containing vacuole, LCV)。磷酸酰肌醇(phosphatidylinositols, PIs)作为细胞的重要脂质组成，参与细胞信号转导及囊泡转运等过程。而大量的证据表明嗜肺军团菌利用其效应蛋白调控宿主磷酸酰肌醇类脂质代谢及其LCV膜的脂质组成，以促进LCV的成熟。本文主要从军团菌的致病机制、其效应蛋白对磷酸酰肌醇类脂质的代谢调控及对宿主磷脂酰肌醇代谢酶的招募等方面进行了综述分析，期望对进一步理解军团菌调控宿主脂质代谢分子机制和其致病机制提供参考。

Abstract:

Legionella pneumophila, the causative agent of the severe pneumonia known as Legionnaires’ disease, uses its IVB secretion system to transport effector proteins into host cells. The effectors interact with host proteins and lipids to form a unique bacterial phagosome, Legionella-containing vacuole (LCV), which is required for the growth of Legionella in host cells. Phosphatidylinositols (PIs), a group of essential lipids for cells, are involved in signal transduction and vesicle transport. The available studies have demonstrated that L. pneumophila uses its effectors to regulate the host PI metabolism and the lipid composition of LCV membrane to promote the LCV maturation. We review the studies about the pathogenesis of L. pneumophila and the modulation of host PI metabolism and the related enzymes by the effectors of L. pneumophila, expecting to provide a reference for further understanding the regulation mechanisms of host lipid metabolism by Legionella.