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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/9599
Title: Soluble intercellular adhesion molecule-1 (ICAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1), and tumor necrosis factor receptor (55 kDa TNF-R) in patients with acute plasmodium falciparum malaria
Authors: C. Wenisch
S. Varijanonta
S. Looareesuwan
W. Graninger
R. Pichler
W. Wernsdorfer
Allgemeines KrankenHaus Wien
Mahidol University
Universitat Wien
Keywords: Immunology and Microbiology;Medicine
Issue Date: 1-Jan-1994
Citation: Clinical Immunology and Immunopathology. Vol.71, No.3 (1994), 344-348
Abstract: Adhesion of Plasmodium falciparum-infected erythrocytes to vascular endothelium is in part mediated by ICAM-1 and ELAM-1 (E-selectin), which can be induced via the 55-kDa TNF-receptor (TNF-R55kDa). We have studied serum levels of soluble ICAM-1 (sICAM-1), ELAM-1 (sELAM-1), and soluble TNF-R55kDa (sTNF-R55kDa) in 37 patients with uncomplicated P. falciparum infection and in 17 control subjects in Bangkok, Thailand. The serum levels of sICAM-1 were markedly elevated in patients prior to treatment (601 ± 239 ng/ml versus 160 ± 47 ng/ml in healthy controls). In addition, elevated levels of sELAM-1 (53.6 ± 23.1 ng/ml versus 21.5 ± 10.1 ng/ml) and sTNF-R5kDa (4.7 ± 3.2 ng/ml versus 1.0 ± 0.4 ng/ml) were observed (P < 0.05 for all). Soluble ELAM-1 reached normal levels on Day 3, and sTNF-R55kDa on Day 14, while sICAM-1 was still significantly elevated 28 days after treatment was started (P < 0.05 for all). A correlation between sTNF-R55kDa (P < 0.05) and sELAM-1 (P < 0.05), respectively, with parasitemia prior to antimalarial treatment was found. These results suggest that a TNF-mediated expression of adhesion molecules induced by the asexual stage of malaria parasites serves as an immune-evasion mechanism. © 1994 Academic Press, Inc.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0028289831&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/9599
ISSN: 00901229
Appears in Collections:Scopus 1991-2000

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