Glycosylphosphatidylinositol toxin of Plasmodium induces nitric oxide synthase expression in macrophages and vascular endothelial cells by a protein tyrosine kinase-dependent and protein kinase C-dependent signaling pathway.

@article{Tachado1996GlycosylphosphatidylinositolTO,
  title={Glycosylphosphatidylinositol toxin of Plasmodium induces nitric oxide synthase expression in macrophages and vascular endothelial cells by a protein tyrosine kinase-dependent and protein kinase C-dependent signaling pathway.},
  author={Souvenir D. Tachado and Peter Gerold and Malcolm J. McConville and Tom Baldwin and D R Quilici and Ralph T. Schwarz and Louis Schofield},
  journal={Journal of immunology},
  year={1996},
  volume={156 5},
  pages={1897-1907}
}
In this study, we demonstrate that glycosylphosphatidylinositol (GPI) is a major toxin of Plasmodium falciparum origin responsible for nitric oxide (NO) production in host cells. Purified malarial GPI is sufficient to induce NO release in a time- and dose-dependent manner in macrophages and vascular endothelial cells, and regulates inducible NO synthase expression in macrophages. GPI-induced NO production was blocked by the NO synthase-specific inhibitor L-N-monomethylarginine. GPI also… CONTINUE READING
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