<Emphasis Type="Italic">Plasmodium falciparum</Emphasis> glycosylphosphatidylinositol induces limited apoptosis in liver and spleen mouse tissue |
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| Authors: | Dominic Wichmann Ralph T Schwarz Volker Ruppert Stephan Ehrhardt Jakob P Cramer Gerd D Burchard Bernhard Maisch Françoise Debierre-Grockiego |
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| Institution: | (1) Bernhard Nocht Institute for Tropical Medicine, Clinical Research Unit, Bernhard-Nocht-Str. 74, 20359 Hamburg, Germany;(2) Institut für Virologie, AG Parasitologie, Hans-Meerwein-Str. 2, D-35043 Marburg, Germany;(3) Hospital of Internal Medicine-Cardiology, Department of Medicine, Laboratory for Cardiac-Immunology, Baldingerstr, 35043 Marburg, Germany;(4) University Hospital Hamburg-Eppendorf, Medical Department I, Tropical Medicine Section, Martinistr., 52, 20246 Hamburg, Germany;(5) University Hospital Ltd. Giessen and Marburg, University Hospital of Internal Medicine-Cardiology Marburg, Baldingerstr, 35043 Marburg, Germany |
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| Abstract: | Plasmodium falciparum malaria affects about 500 million people worldwide and is responsible for approximately 2.5 million deaths per year. Glycosylphosphatidylinositol
(GPI) is the major anchor for membrane-associated proteins of P. falciparum and GPI plays a major role as a toxin in the pathology of malaria. Therefore, we tested the hypothesis that GPI, like LPS,
induces apoptosis in vitro and in vital organs of mice. Our data does not provide evidence for direct cardiomyocyte apoptosis induced by GPI in vitro. However, in vivo injection of GPI induced limited apoptosis in mouse liver and spleen tissue. Apoptosis may be due to a direct GPI apoptotic
effect or to an indirect effect via the induction of TNFα and nitric oxide production. |
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| Keywords: | Apoptosis Cardiomyocytes GPI Heart Plasmodium |
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