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degradation of host sphingomyelin is essential for leishmania virulence降解宿主鞘磷脂对利什曼虫毒性至关重要
Degradation of Host Sphingomyelin Is Essential for Leishmania Virulence 1 1 1 2 2 2 Ou Zhang , Mattie C. Wilson , Wei Xu , Fong-Fu Hsu , John Turk , F. Matthew Kuhlmann , Yingwei 3 3 4 4 1 Wang , Lynn Soong , Phillip Key , Stephen M. Beverley , Kai Zhang * 1 Department of Biological Sciences, Texas Tech University, Lubbock, Texas, United States of America, 2 Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America, 3 Department of Microbiology and Immunology, Department of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States of America, 4 Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, United States of America Abstract In eukaryotes, sphingolipids (SLs) are important membrane components and powerful signaling molecules. In Leishmania, the major group of SLs is inositol phosphorylceramide (IPC), which is common in yeast and Trypanosomatids but absent in mammals. In contrast, sphingomyelin is not synthesized by Leishmania but is abundant in mammals. In the promastigote stage in vitro, Leishmania use SL metabolism as a major pathway to produce ethanolamine (EtN), a metabolite essential for survival and differentiation from non-virulent procyclics to highly virulent metacyclics. To further probe SL metabolism, we identified a gene encoding a putative neutral sphingomyelinase (SMase) and/or IPC hydrolase (IPCase), designated ISCL (Inositol phosphoSphingolipid phospholipase C-Like). Despite the lack of sphingomyelin synthesis, L. major promastigotes exhibited a potent SMase activity which was a
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