Fischer K, Chatterjee D, Torrelles J, Brennan P J, Kaufmann S H, Schaible U E
Max-Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany.
J Immunol. 2001 Aug 15;167(4):2187-92. doi: 10.4049/jimmunol.167.4.2187.
Pathogenic mycobacteria are able to survive and proliferate in phagosomes within host macrophages (Mphi). This capability has been attributed in part to their cell wall, which consists of various unique lipids. Some of these are important in the host-pathogen interaction, such as resistance against microbicidal effector mechanisms and modulation of host cell functions, and/or are presented as Ags to T cells. Here we show that two lipids are released from the mycobacterial cell wall within the phagosome of infected Mphi and transported out of this compartment into intracellular vesicles. One of these lipids was identified as lysocardiolipin. Lysocardiolipin was generated through cleavage of mycobacterial cardiolipin by a Ca2+-independent phospholipase A2 present in Mphi lysosomes. This result indicates that lysosomal host cell enzymes can interact with released mycobacterial lipids to generate new products with a different intracellular distribution. This represents a novel pathway for the modification of bacterial lipid Ags.
致病性分枝杆菌能够在宿主巨噬细胞（Mphi）内的吞噬体中存活和增殖。这种能力部分归因于其细胞壁，细胞壁由各种独特的脂质组成。其中一些脂质在宿主-病原体相互作用中很重要，例如抵抗杀菌效应机制和调节宿主细胞功能，和/或作为抗原呈递给T细胞。在这里，我们展示了两种脂质从感染Mphi的吞噬体内的分枝杆菌细胞壁释放出来，并从这个区室转运到细胞内囊泡中。其中一种脂质被鉴定为溶血心磷脂。溶血心磷脂是由Mphi溶酶体中存在的一种不依赖Ca2+的磷脂酶A2切割分枝杆菌心磷脂产生的。这一结果表明，溶酶体宿主细胞酶可以与释放的分枝杆菌脂质相互作用，产生具有不同细胞内分布的新产物。这代表了一种修饰细菌抗原的新途径。
