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首页> 外文期刊>Journal of Parasitology >PROINFLAMMATORY CYTOKINES IN GRANULOMAS ASSOCIATED WITH MURINE CYSTICERCOSIS ARE NOT THE CAUSE OF SEIZURES
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PROINFLAMMATORY CYTOKINES IN GRANULOMAS ASSOCIATED WITH MURINE CYSTICERCOSIS ARE NOT THE CAUSE OF SEIZURES

机译：鼠囊性囊病相关的肉芽肿中抑菌性细胞因子并非诱因

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Neurocysticercosis is a parasitic infection of the human central nervous system caused by the cestode Taenia solium. The most common clinical manifestations of neurocysticercosis are seizures. Taenia crassiceps cysticercosis in mice has been used as an experimental model for T. solium cysticercosis. Granulomas surrounding murine cysticerci have striking immunopathological resemblance to human neurocysticercosis; early stage granulomas were able to induce seizures in a rodent model. To assess the role of proinflammatory cytokines in early stage granulomas, we isolated RNA from murine cysticercal granulomas and checked for cytokine expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and/or ribonuclease (RNase) protection assays. Cytokine expression was compared with histological stages. Interleukin (IL)-1α, IL-1β, IL-1 receptor antagonist, and tumor necrosis factor (TNF-α) were the major cytokines detected in all granulomas. Signals for IL-12, IL-18, and IL-6 RNA were not consistently detected and, when detected, were barely demonstrable. Expression of migration inhibitory factor (MIF), IL-6, IL-1α, TNF-α, and IL-18 was not significantly different between early and late-stage granulomas. Expression of IL-1β, IL-1 receptor antagonist, and IL-12 p40 were higher in late, compared with early, stages. Thus, we demonstrated a broad range of cytokines in these granulomas. However, we did not document preferential expression of any proinflammatory cytokines in early stage granulomas. Thus, proinflammatory cytokines are not responsible for the seizures in the rodent model of neurocysticercosis.
机译：神经囊尾osis病是由c虫Ta虫en虫引起的人中枢神经系统的寄生虫感染。神经囊尾rc病最常见的临床表现是癫痫发作。小鼠中的Taenia crassiceps囊尾rc病已被用作T. solium囊尾rc病的实验模型。鼠类囊尾er周围的肉芽肿与人神经囊尾rc病具有惊人的免疫病理学相似性；早期肉芽肿能够在啮齿动物模型中诱发癫痫发作。为了评估促炎细胞因子在早期肉芽肿中的作用，我们从鼠类囊性肉芽肿中分离了RNA，并通过逆转录聚合酶链反应（RT-PCR）和/或核糖核酸酶（RNase）保护试验检测了细胞因子的表达。将细胞因子的表达与组织学阶段进行比较。白细胞介素（IL）-1α，IL-1β，IL-1受体拮抗剂和肿瘤坏死因子（TNF-α）是在所有肉芽肿中检测到的主要细胞因子。 IL-12，IL-18和IL-6 RNA的信号无法持续检测到，并且在检测到时几乎无法显示。早期和晚期肉芽肿之间迁移抑制因子（MIF），IL-6，IL-1α，TNF-α和IL-18的表达无明显差异。与早期相比，IL-1β，IL-1受体拮抗剂和IL-12 p40的表达在后期较高。因此，我们证明了在这些肉芽肿中广泛的细胞因子。但是，我们没有记录早期肉芽肿中任何促炎细胞因子的优先表达。因此，在神经囊尾osis病的啮齿动物模型中，促炎细胞因子与癫痫发作无关。

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