Goren M B, D'Arcy Hart P, Young M R, Armstrong J A
Proc Natl Acad Sci U S A. 1976 Jul;73(7):2510-4. doi: 10.1073/pnas.73.7.2510.
Intracellular parasites (e.g., Mycobacterium tuberculosis, Toxoplasma gondii, and some Chlamydiae) may promote their survival within the host by acting from within phagosomes to prevent phagolysosome formation, thus avoiding exposure to the lysosomal hydrolases. The present studies demonstrate that when sulfatides of M. tuberculosis (anionic trehalose glycolipids largely responsible for the neutral red reactivity of virulent strains) are administered to cultured mouse peritoneal macrophages, they accumulate in the secondary lysosomes, which are rendered incompetent for fusion with phagosomes containing suitable target particles such as viable yeasts. This antifusion effect is also exhibited when small amounts of sulfatide are introduced directly into phagosomes by attachment to the target yeasts prior to their ingestion. The sulfatides evidently exert a selective inhibitory influence on membrane fusion, analogous to what occurs typically when macrophage cultures are infected with tubercle bacilli. This effect may be due to ionic interaction between the polyanionic micelles of bacterial sulfatide and organelle membranes, modifying the latter and inducing dysfunction.
细胞内寄生虫（如结核分枝杆菌、弓形虫和某些衣原体）可能通过在吞噬体内发挥作用来阻止吞噬溶酶体的形成，从而避免暴露于溶酶体水解酶，以此促进它们在宿主体内的存活。目前的研究表明，当将结核分枝杆菌的硫脂（一种主要负责有毒菌株中性红反应性的阴离子海藻糖糖脂）施用于培养的小鼠腹腔巨噬细胞时，它们会在次级溶酶体中积累，这些次级溶酶体无法与含有合适靶颗粒（如活酵母）的吞噬体融合。当在吞噬之前将少量硫脂通过附着在靶酵母上直接引入吞噬体时，也会表现出这种抗融合作用。硫脂显然对膜融合发挥了选择性抑制作用，类似于巨噬细胞培养物感染结核杆菌时通常发生的情况。这种作用可能是由于细菌硫脂的聚阴离子胶束与细胞器膜之间的离子相互作用，改变了后者并导致功能障碍。
