Open AccessGreater Endothelial Activation, Weibel‐Palade Body Release and Host Inflammatory Response toPlasmodium vivax,Compared withPlasmodium falciparum: A Prospective Study in Papua, Indonesia
Author(s) -
Tsin Wen Yeo,
Daniel A. Lampah,
Emiliana Tjitra,
Kim A. Piera,
Retno Gitawati,
Enny Kenangalem,
Ric N. Price,
Nicholas M. Anstey
Publication year - 2010
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/653211
Subject(s) - plasmodium falciparum , plasmodium vivax , host (biology) , biology , malaria , plasmodium (life cycle) , immunology , apicomplexa , parasite hosting , virology , medicine , genetics , world wide web , computer science
Pathogenic mechanisms underlying vivax malaria are poorly understood, with few studies comparing endothelial and inflammatory responses with falciparum malaria. In adults with uncomplicated vivax or falciparum malaria, we compared plasma measurements of endothelial Weibel-Palade body release (angiopoietin-2) and activation (ICAM-1, E-selectin), as well as selected cytokines. Despite a lower median parasite count, angiopoietin-2 concentrations were higher in patients with vivax malaria, compared with falciparum malaria. Per peripheral parasite, median plasma angiopoietin-2, ICAM-1, E-selectin, interleukin-6, and interleukin-10 concentrations were higher in patients with malaria due to Plasmodium vivax. P. vivax induces greater endothelial Weibel-Palade body release and activation and greater host inflammatory responses, compared with Plasmodium falciparum.
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