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首页> 外文期刊>International 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.
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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.

机译：小鼠对疟疾易感或耐药的品系中的细胞因子和趋化因子对伯氏疟原虫ANKA感染的反应：大脑中早期趋化因子的表达。

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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 approximately 15-20% with cerebral symptoms, while BALB/c mice survived until week 3 after infection. Although both strains showed T(h)1-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 T(h)1 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.
机译：对在伯氏疟原虫ANKA感染的脑疟疾（CM）易感或耐药小鼠（分别为C57BL / 6或BALB / c）小鼠中的细胞因子和趋化因子反应进行了比较研究。 C57BL / 6小鼠在感染后10天死亡，当时伴有脑部症状的寄生虫病率约为15-20％，而BALB / c小鼠存活到感染后第3周。尽管两种菌株在感染后第4天均显示出T（h）1偏斜反应，但在感染过程中BALB / c中观察到了明显更高的IFN-γ，肿瘤坏死因子（TNF）-α和NO水平，这表明T（h）1响应与阻力有关。有趣的是，在脑中，这两种菌株早在感染后24小时就表达了10kDa（IP-10）的IFN诱导型蛋白和单核细胞趋化蛋白（MCP）-1基因，而此后这两种菌株之间都观察到了一些差异，即RANTES在C57BL / 6中的表达增强，而IFN-γ和TNF-α在BALB / c中的表达增强。此外，在体外用疟原虫的粗制抗原刺激诱导了星形胶质细胞系KT-5中IP-10和MCP-1基因的表达。这些结果表明，脑实质细胞直接参与了对疟原虫的感染，为分析CM的可能机制提供了新的方面。这是关于疟疾感染后神经胶质细胞趋化因子表达的首次报道。

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