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首页> 外文期刊>Infection and immunity >Detoxified exoantigens and phosphatidylinositol derivatives inhibit tumor necrosis factor induction by malarial exoantigens.
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Detoxified exoantigens and phosphatidylinositol derivatives inhibit tumor necrosis factor induction by malarial exoantigens.

机译：排毒的外源抗原和磷脂酰肌醇衍生物可抑制疟疾外源抗原诱导的肿瘤坏死因子诱导。

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We have previously shown that malaria parasites liberate exoantigens which, through a phospholipid component, stimulate mouse macrophages to secrete tumor necrosis factor (TNF), which are toxic to D-galactosamine-sensitized mice, and which therefore might be involved in pathology. Plasmodium yoelii exoantigens detoxified by dephosphorylation or digestion with lipases do not induce TNF production. However, these partial structures inhibited its production in response to the exoantigens, although not to bacterial lipopolysaccharide (LPS). When pure phospholipids were tested in a macrophage assay, none stimulated the production of TNF, but phosphatidylinositol (PI) inhibited TNF induction by P. yoelii exoantigens. Moreover, inositol monophosphate (IMP) was the only one of a number of monophosphate saccharides tested which was inhibitory; inositol was not. Macrophages pretreated with PI, IMP, or detoxified exoantigens and then incubated with parasite exoantigens also yielded much less TNF. PI, IMP, and lipase-digested exoantigens of P. yoelii similarly inhibited the TNF-inducing activity of exoantigens of the human parasites Plasmodium falciparum and Plasmodium vivax. Neither PI nor IMP diminished TNF production in response to LPS, in contrast to a platelet-activating factor antagonist [1-O-hexadecyl-2-acetyl- sn-glycero-3-phospho(N,N,N-trimethyl hexanolamine)] which inhibited both exoantigen- and LPS-induced production of TNF. We conclude that at least two different parts of the molecule are involved in the induction of TNF secretion by parasite exoantigens: one requires the presence of a phosphate bound to inositol, and, since dephosphorylated exoantigens were also inhibitory, one does not. It would seem that both affect interactions between parasite-derived exoantigens and the macrophage receptors.
机译：以前我们已经表明，疟疾寄生虫会释放外源抗原，后者通过磷脂成分刺激小鼠巨噬细胞分泌对N-半乳糖胺致敏的小鼠有毒的肿瘤坏死因子（TNF），因此可能与病理有关。通过去磷酸化或用脂肪酶消化而解毒的约氏疟原虫外抗原不诱导TNF产生。然而，这些部分结构抑制了其对外源抗原的产生，尽管对细菌脂多糖（LPS）没有作用。当在巨噬细胞测定法中测试纯磷脂时，没有一个刺激刺激TNF的产生，但是磷脂酰肌醇（PI）抑制了约氏疟原虫外抗原对TNF的诱导。此外，肌醇单磷酸酯（IMP）是测试的多种单磷酸糖中唯一具有抑制作用的糖。肌醇不是。用PI，IMP或解毒的外源抗原预处理的巨噬细胞，然后与寄生虫外源抗原一起孵育，产生的TNF也要少得多。 PI，IMP和约瑟氏酵母脂肪酶消化的外源抗原同样抑制人寄生虫恶性疟原虫和间日疟原虫的外源抗原的TNF诱导活性。与血小板活化因子拮抗剂[1-O-十六烷基-2-乙酰基-sn-甘油-3-磷酸（N，N，N-三甲基己醇胺）相反，PI和IMP均不能降低对LPS的TNF产生。抑制外源抗原和LPS诱导的TNF产生。我们得出的结论是，该分子的至少两个不同部分参与了寄生虫外源抗原的TNF分泌诱导：一个需要结合肌醇的磷酸盐存在，而由于去磷酸化的外源抗原也具有抑制作用，所以一个则不具有抑制作用。似乎两者都影响寄生虫来源的外抗原和巨噬细胞受体之间的相互作用。

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