Regulation of Leukocyte Adhesion Molecules CD11b/CD18 and Leukocyte Adhesion Molecule-1 on Phagocytic Cells Activated by Malaria Pigment

S. Pichyangkul Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand

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P. Saengkrai Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand

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K. Yongvanitchit Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand

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D. G. Heppner Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand

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D. E. Kyle Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand

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H. K. Webster Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand

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DOI:
https://doi.org/10.4269/ajtmh.1997.57.383
Volume/Issue:
Volume 57: Issue 4
Page(s):
383–388
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There is increasing evidence that inappropriate immune activation induced by parasite products occurs in malaria disease. To further clucidate the role of Plasmodium falciparum-derived products on host immune activation, we studied the expression of leukocyte adhesion molecules (CD11b/CD18 and LAM-1) on neutrophils and monocytes in response to malaria pigment using flow cytometry. Exposure of leukocytes to isolated malaria pigment derived from ruptured schizonts resulted in significant up-regulation of CD11b/CD18 expression and down-regulation of LAM-1 on both neutrophils and monocytes. In contrast, culture supernatants (pigment free) from ruptured schizonts did not alter the expression of CD11b/CD18 and LAM-1. The increase of CD11b/CD18 and the loss of LAM-1 expression occurred simultaneously with the earliest response detected at 10 min and a plateau reached by 60 min. The effect of malaria pigment on leukocyte adhesion molecules was inhibited by EDTA in a dose-dependent manner. Phagocytosis of malaria pigment was also suppressed by EDTA. This observation suggests that phagocytosis of malaria pigment may be a prerequisite for the effect of malaria pigment on the regulation of CD11b/CD18 and LAM-1 expression. Regulation of leukocyte adhesion molecules through up-regulation of CD11b/CD18 and down-regulation of LAM-1 by malaria pigment could promote leukocyte adherence to endothelium in vivo. This increased adherence of malaria pigment-activated leukocytes might induce cytokine (tumor necrosis factorα and interleukin-1β)-mediated increases in capillary permeability resulting in local tissue edema, and a cytokine-mediated increase in adhesion molecule expression causing vascular clogging by adherent red blood cells, and in severe disease by adherent leukocytes.

Author Notes

Copyright:
Copyright © 1997 by The American Society of Tropical Medicine and Hygiene 1997
Published Online:
Oct 1997
Cover The American Journal of Tropical Medicine and Hygiene
The American Journal of Tropical Medicine and Hygiene
Print ISSN:
0002-9637
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