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首页> 美国卫生研究院文献>Infection and Immunity >Optimal Tumor Necrosis Factor Induction by Plasmodium falciparum Requires the Highly Localized Release of Parasite Products
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Optimal Tumor Necrosis Factor Induction by Plasmodium falciparum Requires the Highly Localized Release of Parasite Products

机译：恶性疟原虫的最佳肿瘤坏死因子诱导需要高度局部释放的寄生虫产品。

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Overproduction of tumor necrosis factor (TNF) has been linked with the pathogenesis of Plasmodium falciparum malaria. Here, we examined why the high levels of TNF-inducing activity associated with P. falciparum-parasitized erythrocytes (PE) appear to be lost after cell lysis. Static coculture of PE and peripheral blood mononuclear cells (PBMC), with or without separation by porous membranes, demonstrated that rupture of live PE in the presence of responder cells was required for optimal TNF induction. Although the insoluble fraction of lysed PE was found to partially inhibit TNF responses, supernatants prepared from large numbers of lysed PE still contained only low levels of TNF-inducing activity, which showed no evidence of instability. A dramatic reduction in TNF levels resulted when noncytoadherent PE lines were maintained under low-cell-proximity conditions by suspension coculture. This reduction was much less marked with PE capable of adhering to PBMC, despite the fact that cytoadherent and noncytoadherent parasite lines induced comparable levels of TNF in high-cell-proximity, static coculture. These results suggest that rupture of PE in a highly localized setting, facilitated by either static coculture or the more biologically relevant phenomenon of cytoadherence to PBMC, can result in considerable enhancement of the P. falciparum-induced TNF response.
机译：肿瘤坏死因子（TNF）的过度生产与恶性疟原虫疟疾的发病机理有关。在这里，我们检查了为什么细胞裂解后与恶性疟原虫寄生红细胞（PE）相关的高水平的TNF诱导活性似乎消失了。 PE和外周血单核细胞（PBMC）的静态共培养，无论是否通过多孔膜分离，都证明了在有应答细胞的情况下活PE的破裂对于最佳的TNF诱导是必需的。尽管发现裂解的PE的不溶部分可部分抑制TNF反应，但从大量裂解的PE制备的上清液仍仅包含低水平的TNF诱导活性，这没有显示出不稳定的迹象。当通过悬浮共培养将非细胞粘附性PE品系维持在低细胞接近性条件下时，TNF水平显着降低。尽管在高细胞邻近度，静态共培养中，细胞粘附和非细胞粘附的寄生物系可诱导相当水平的TNF，但这种粘附能力却很少能与PBMC粘附。这些结果表明，通过静态共培养或与PBMC发生细胞粘附的生物学上更相关的现象所促进的高度局限性PE破裂，可导致恶性疟原虫诱导的TNF反应显着增强。

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