Open AccessNeutrophils play a critical role in the pathogenesis of experimental cerebral malaria
Author(s) -
Chen L.,
Zhang Z.H.,
Sendo F.
Publication year - 2000
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.2000.01196.x
Subject(s) - plasmodium berghei , pathogenesis , cerebral malaria , immunology , biology , tumor necrosis factor alpha , immune system , cytokine , interferon gamma , spleen , proinflammatory cytokine , interferon , reverse transcriptase , malaria , inflammation , plasmodium falciparum , polymerase chain reaction , gene , biochemistry
The role of neutrophils in experimental cerebral malaria (ECM) is not well understood. In this study we used a MoAb, RB6‐8C5, to deplete the peripheral neutrophils of ECM‐susceptible CBA/NSlc mice 24 h before Plasmodium berghei ANKA (PbA) infection. We found that early neutrophil depletion prevented the development of ECM and dramatically decreased the sequestration of monocytes and microhaemorrhage in the brain. The depletion of neutrophils also down‐regulated tumour necrosis factor‐alpha, interferon‐gamma and IL‐2 mRNAs and abrogated IL‐12p40 mRNA expression in the brain as examined by competitive reverse transcriptase‐polymerase chain reaction. Although depletion of neutrophils decreased the expression of Th1 cytokines in both spleen and brain, our results did not show the shift of a Th1 to a Th2 immune response since there was no obvious augmentation of expression of Th2 cytokine mRNAs (IL‐4 and IL‐10). We conclude that neutrophils play a role in the pathogenesis of ECM via enhancement of the expression of Th1 cytokines in the brain.
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