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Originally published In Press as doi:10.1074/jbc.C100007200 on January 10, 2001

J. Biol. Chem., Vol. 276, Issue 10, 6909-6912, March 9, 2001
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ACCELERATED PUBLICATION
Plasmodium falciparum Glycosylphosphatidylinositol-induced TNF-alpha Secretion by Macrophages Is Mediated without Membrane Insertion or Endocytosis*

Matam Vijaykumar, Ramachandra S. Naik, and D. Channe GowdaDagger

From the Department of Biochemistry and Molecular Biology, Georgetown University Medical Center, Washington, D. C. 20007

The glycosylphosphatidylinositols (GPIs) of Plasmodium falciparum are believed to contribute to the pathogenesis of malaria by inducing the secretion of proinflammatory cytokines by macrophages. Previous studies have shown that P. falciparum GPIs elicit toxic immune responses by protein tyrosine kinase (PTK)- and protein kinase C (PKC)-mediated cell signaling pathways, which are activated by the carbohydrate and acyl moieties of the intact GPIs, respectively. In this study, we show that induction of TNF-alpha by P. falciparum GPIs in macrophages is mediated by the recognition of the distal fourth mannose residue. This event is critical but not sufficient for the productive cell signaling; interaction by the acylglycerol moiety of GPIs is also required. These novel interactions are coupled to previously demonstrated PTK and PKC pathways, since the specific inhibitors of these kinases effectively blocked the GPI-induced TNF-alpha production. Surprisingly, sn-2 lyso-GPIs were also able to elicit TNF-alpha secretion. Contrary to the prevailing notion, GPIs are neither inserted to the plasma membranes nor endocytosized. Thus, this study defines the GPI structural requirements and reveals a novel mechanism for the outside-in activation of cell signaling by P. falciparum GPIs in inducing proinflammatory responses.

* This study was supported by Grant AI41139 from NIAID, National Institutes of Health.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Dept. of Biochemistry and Molecular Biology, 3900 Reservoir Rd., N. W., Washington, D. C. 20007. Tel.: 202-687-3840; Fax: 202-687-7186; E-mail: gowda@bc.georgetown.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.