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.

Open Access
Publisher Website
Google Scholar
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.

This publication has 0 references indexed in Scilit: