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首页> 外文期刊>Tropical biomedicine. >Modulation of interleukin-18 release produced positive outcomes on parasitaemia development and cytokines production during malaria in mice
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Modulation of interleukin-18 release produced positive outcomes on parasitaemia development and cytokines production during malaria in mice

机译：白细胞介素18释放的调节对疟疾在小鼠中的寄生虫血症的发展和细胞因子的产生产生积极的结果

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The involvement of interleukin-18 (IL-18) and the effects of modulating its release on the course of malaria infection were investigated using Plasmodium berghei ANKA infection in ICR mice as a model. Results demonstrated that plasma IL-18 concentrations in malarial mice were significantly elevated and positively correlated with the percentage parasitaemia development. Significant expressions of IL-18 were also observed in the brain, spleen and liver tissues. Slower development of parasitaemia was observed significantly upon inhibition and neutralization of IL-18, whereas faster development of parasitaemia was recorded when the circulating levels of IL-18 were further augmented during the infection. Inhibition and neutralization of IL-18 production also resulted in a significant decrease of plasma concentrations of pro-inflammatory cytokines (TNFα, IFNγ, IL-1α and IL-6), whereas the anti-inflammatory cytokine, IL-10, was significantly increased. Augmenting the release of IL-18 during the infection on the other hand resulted in the opposite. Early mortality in malarial mice was also observed when the circulating levels of IL-18 were further augmented. Results proved the important role of IL-18 in immune response against malaria and suggest that IL-8 is pro-inflammatory in nature and may involve in mediating the severity of the infection through a pathway of elevating the pro-inflammatory cytokine and limiting the release of anti-inflammatory cytokine.
机译：以ICR小鼠中的伯氏疟原虫ANKA感染为模型，研究了白介素18（IL-18）的参与及其在疟疾感染过程中调节其释放的作用。结果表明，疟疾小鼠的血浆IL-18浓度显着升高，并且与寄生虫血症的发生率呈正相关。在脑，脾和肝组织中也观察到IL-18的重要表达。通过抑制和中和IL-18，可明显观察到寄生虫病的发生较慢，而在感染过程中，当IL-18的循环水平进一步升高时，寄生虫病的发生会更快。 IL-18产生的抑制和中和还导致促炎细胞因子（TNFα，IFNγ，IL-1α和IL-6）的血浆浓度显着降低，而抗炎细胞因子IL-10显着增加。另一方面，在感染期间增加IL-18的释放导致相反的结果。当IL-18的循环水平进一步提高时，也观察到了疟疾小鼠的早期死亡。结果证明了IL-18在针对疟疾的免疫应答中的重要作用，并暗示IL-8本质上是促炎性的，并且可能通过升高促炎性细胞因子和限制释放的途径来介导感染的严重性。抗炎细胞因子。

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