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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/11436
Title: Digestive vacuoles of Plasmodium falciparum are selectively phagocytosed by and impair killing function of polymorphonuclear leukocytes
Authors: Prasad Dasari
Karina Reiss
Klaus Lingelbach
Stefan Baumeister
Ralph Lucius
Rachanee Udomsangpetch
Sebastian Chakrit Bhakdi
Sucharit Bhakdi
Klinikum der Johannes-Gutenberg-Universitat und Fachbereich Medizin
Christian-Albrechts-Universitat zu Kiel
Universitat Marburg
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology;Medicine
Issue Date: 3-Nov-2011
Citation: Blood. Vol.118, No.18 (2011), 4946-4956
Abstract: Sequestration of parasitized erythrocytes and dysregulation of the coagulation and complement system are hallmarks of severe Plasmodium falciparum malaria. A link between these events emerged through the discovery that the parasite digestive vacuole (DV), which is released together with infective merozoites into the bloodstream, dually activates the intrinsic clotting and alternative complement pathway. Complement attack occurs exclusively on the membrane of the DVs, and the question followed whether DVs might be marked for uptake by polymorphonuclear granulocytes (PMNs). We report that DVs are indeed rapidly phagocytosed by PMNs after schizont rupture in active human serum. Uptake of malaria pigment requires an intact DV membrane and does not occur when the pigment is extracted from the organelle. Merozoites are not opsonized and escape phagocytosis in nonimmune serum. Antimalarial Abs mediate some uptake of the parasites, but to an extent that is not sufficient to markedly reduce reinvasion rates. Phagocytosis of DVs induces a vigorous respiratory burst that drives the cells into a state of functional exhaustion, blunting the production of reactive oxygen species (ROS) and microbicidal activity upon challenge with bacterial pathogens. Systemic overloading of PMNs with DVs may contribute to the enhanced susceptibility of patients with severe malaria toward invasive bacterial infections. © 2011 by The American Society of Hematology.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=80855144793&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/11436
ISSN: 15280020
00064971
Appears in Collections:Scopus 2011-2015

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