Fatty acids from Plasmodium falciparum down-regulate the toxic activity of malaria glycosylphosphatidylinositols
Details
Publication Year 2006-10,Volume 74,Issue #10,Page 5487-5496
Journal Title
INFECTION AND IMMUNITY
Publication Type
Journal Article
Abstract
Plasmodium falciparum malaria kills roughly 2.5 million people, mainly children, annually. Much of this mortality is thought to arise from the actions of a malarial toxin. This toxin, identified as glycosylphosphatidylinositol (GPI), is a major pathogenicity determinant in malaria. A malarial molecule, Pfj, labeled by [H-3]glucosamine like the GPIs, was identified as a non-GPI molecule. Here we show that Pfj is able to down-regulate tumor necrosis factor alpha (TNF-alpha) production induced by the GPI of P. falciparum. Mass spectrometry analysis showed that Pfj was not a single molecule but represented a number of molecules. Separation methods, such as cation-exchange chromatography and thin-layer chromatography, were used to isolate and identify the following four main fatty acids responsible for the inhibitory effect on TNF-alpha production: myristic, pentadecanoic, palmitic, and palmitoleic acids. This regulatory effect on cytokine production suggests that there is balanced bioactivity for the different categories of malarial lipids.
Publisher
AMER SOC MICROBIOLOGY
Keywords
ASEXUAL ERYTHROCYTIC STAGES; VASCULAR ENDOTHELIAL-CELLS; CONJUGATED LINOLEIC-ACID; FACTOR-ALPHA PRODUCTION; PROTEIN-KINASE-C; INFECTED ERYTHROCYTES; PARASITIZED ERYTHROCYTES; SIGNAL-TRANSDUCTION; MEMBRANE ANCHOR; PPAR-ALPHA
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Creation Date: 2006-10-01 12:00:00
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