Publication: Cytokine and chemokine responses in a cerebral malaria-susceptible or -resistant strain of mice to Plasmodium berghei ANKA infection: Early chemokine expression in the brain
Issued Date
2003-05-01
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ISSN
09538178
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2-s2.0-0037407318
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Mahidol University
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SCOPUS
Bibliographic Citation
International Immunology. Vol.15, No.5 (2003), 633-640
Suggested Citation
Syarifah P. Hanum, Masashi Hayano, Somei Kojima Cytokine and chemokine responses in a cerebral malaria-susceptible or -resistant strain of mice to Plasmodium berghei ANKA infection: Early chemokine expression in the brain. International Immunology. Vol.15, No.5 (2003), 633-640. doi:10.1093/intimm/dxg065 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/20904
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Title
Cytokine and chemokine responses in a cerebral malaria-susceptible or -resistant strain of mice to Plasmodium berghei ANKA infection: Early chemokine expression in the brain
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Abstract
A comparative study was carried out on cytokine and chemokine responses in a cerebral malaria (CM)-susceptible or -resistant strain of mice (C57BL/6 or BALB/c respectively) in Plasmodium berghei ANKA infection. C57BL/6 mice died by 10 days after infection when parasitemia was ∼15-20% with cerebral symptoms, while BALB/c mice survived until week 3 after infection. Although both strains showed Th1-skewed responses on day 4 after infection, significantly higher levels of IFN-γ, tumor necrosis factor (TNF)-α and NO were observed during the course of the infection in BALB/c, suggesting that Th1 responses are involved in the resistance. Interestingly, in the brain, both strains expressed IFN-inducible protein of 10 kDa (IP-10) and monocyte chemotactic protein (MCP)-1 genes as early as at 24 h post-infection, whereas some differences were observed between both strains thereafter, i.e. enhanced expression of RANTES in C57BL/6, and of IFN-γ and TNF-α in BALB/c respectively. Moreover, the expression of IP-10 and MCP-1 genes in KT-5, an astrocyte cell line, was induced in vitro upon stimulation with a crude antigen of malaria parasites. These results suggest that the direct involvement of brain parenchymal cells takes place in response to plasmodial infection, providing a new aspect to analyze possible mechanisms of CM. This is the first report on the chemokine expression in neuroglial cells in response to malaria infection.