Publication Date:
2009-02-07
Description:
Platelets play a critical role in the pathogenesis of malarial infections by encouraging the sequestration of infected red blood cells within the cerebral vasculature. But platelets also have well-established roles in innate protection against microbial infections. We found that purified human platelets killed Plasmodium falciparum parasites cultured in red blood cells. Inhibition of platelet function by aspirin and other platelet inhibitors abrogated the lethal effect human platelets exert on P. falciparum parasites. Likewise, platelet-deficient and aspirin-treated mice were more susceptible to death during erythrocytic infection with Plasmodium chabaudi. Both mouse and human platelets bind malarial-infected red cells and kill the parasite within. These results indicate a protective function for platelets in the early stages of erythrocytic infection distinct from their role in cerebral malaria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMorran, Brendan J -- Marshall, Vikki M -- de Graaf, Carolyn -- Drysdale, Karen E -- Shabbar, Meriam -- Smyth, Gordon K -- Corbin, Jason E -- Alexander, Warren S -- Foote, Simon J -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):797-800. doi: 10.1126/science.1166296.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Menzies Research Institute, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. brendan.mcmorran@utas.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19197068" target="_blank"〉PubMed〈/a〉
Keywords:
Adenosine Diphosphate/metabolism
;
Animals
;
Aspirin/pharmacology
;
Blood Platelets/metabolism/*physiology
;
Erythrocytes/*parasitology
;
Female
;
Humans
;
In Situ Nick-End Labeling
;
Malaria/*blood/immunology/*parasitology
;
Male
;
Mice
;
Mice, Inbred C57BL
;
Mice, Knockout
;
Plasmodium chabaudi/*growth & development
;
Plasmodium falciparum/*growth & development
;
Platelet Activation
;
Platelet Aggregation Inhibitors/pharmacology
;
Platelet Count
;
Receptors, Purinergic P2/metabolism
;
Receptors, Purinergic P2Y1
;
Receptors, Thrombopoietin/genetics
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
