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International Immunology, Vol. 15, No. 5, pp. 633-640, May 2003
© 2003 Japanese Society for Immunology

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

Syarifah Hanum P.1, Masashi Hayano1 and Somei Kojima1,2,3

1 Department of Parasitology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan 2 Department of Parasitology, Tokyo Medical University, Tokyo 160-8402, Japan 3 Present address: Asian Centre of International Parasite Control, Faculty of Tropical Medicine, Mahidol University, Bangkok 10400, Thailand

Correspondence to: S. Kojima, Asian Centre of International Parasite Control, Faculty of Tropical Medicine, Mahidol University, 420/6 Ratchawithi Road, Bangkok 10400, Thailand. E-mail: fnskj{at}diamond.mahidol.ac.th
Transmitting editor: S. Koyasu

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-{gamma}, tumor necrosis factor (TNF)-{alpha} 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-{gamma} and TNF-{alpha} 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.

Keywords: astrocyte, cerebral malaria, chemokine, cytokine, Plasmodium berghei


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