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Apoptosis: a potential triggering mechanism of neurological manifestation in Plasmodium falciparum malaria
Author(s) -
TOURÉ F. S.,
OUWEMISSIOUKEMBOYER O.,
BISVIGOU U.,
MOUSSA O.,
ROGIER C.,
PINO P.,
MAZIER D.,
BISSER S.
Publication year - 2008
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2007.00986.x
Subject(s) - plasmodium falciparum , biology , malaria , apoptosis , pathogenesis , immunology , disease , parasite hosting , plasmodium (life cycle) , mechanism (biology) , genetics , pathology , medicine , computer science , world wide web , philosophy , epistemology
SUMMARY Plasmodium falciparum infection can lead to a life threatening disease and the pathogenetic mechanisms of severe manifestations are not fully understood. Here, we investigated the capacity of P. falciparum ‐parasitized red blood cells (PRBC) from 45 children with clinical malaria to induce endothelial cell (EC) apoptosis.In all subjects, PRBC that cytoadhered to ECs could be found albeit to a variable degree. By contrast, PRBC that induce EC apoptosis were found only in nine (20%) subjects. Interestingly, children with neurological manifestations were significantly more likely to harbour apoptogenic strains. There was no quantitative relationship between the capacity of these isolates to cytoadhere and apoptosis induction. We hypothesize that P. falciparum ‐encoded molecules could be responsible for apoptosis induction and therefore suggest new insights in the pathogenesis of P. falciparum malaria. Further investigations are currently in progress to determine whether these results can be confirmed and to identify putative parasite apoptogenic factors.