RECOMBINANT C5A ENHANCES INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR RELEASE BY LIPOPOLYSACCHARIDE-STIMULATED MONOCYTES AND MACROPHAGES
RECOMBINANT C5A ENHANCES INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR RELEASE BY LIPOPOLYSACCHARIDE-STIMULATED MONOCYTES AND MACROPHAGES
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DOI：
10.1002/eji.1830200204
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发表时间：
1990-02-01
影响因子：
5.4
通讯作者：
HAEFFNERCAVAILLON, N
中科院分区：
文献类型：
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作者：
CAVAILLON, JM;FITTING, C;HAEFFNERCAVAILLON, N
脂多糖（LPS）是一种强有力的诱导白细胞介素1（IL 1）的合成和释放，以及肿瘤坏死因子（TNF）的分泌。许多信号可以增强LPS诱导的这些细胞因子的产生。我们以前观察到，在培养基中加入少量的正常人血清可增强IL 1的产生。在血清因子中，过敏毒素C3 a和C5 a和/或它们的desArg衍生物已显示出增强LPS诱导的IL 1和TNF产生。然而，天然过敏毒素本身诱导细胞因子产生的能力仍然是一个有争议的问题。我们研究了人重组C5 a（hrC 5a）诱导IL 1和TNF产生的能力。尽管缺乏直接触发，hrC 5a能够与LPS协同作用，导致人单核细胞和小鼠腹腔巨噬细胞释放更高的IL 1和TNF。如通过共有丝分裂试验所评估的，hrC 5a增加IL 1释放，而细胞相关的IL 1活性没有显著改变。通过酶联免疫吸附测定法测量人IL 1 β导致了类似的结论，而IL 1 α的测量。通过放射免疫测定表明，此外，细胞内IL 1 α增加。
Lipopolysaccharide (LPS) is a potent inducer of interleukin 1 (IL 1) synthesis and release, and of tumor necrosis factor (TNF) secretion. Many signals can enhance the LPS-induced production of these cytokines. We have previously observed that addition of low amounts of normal human serum to the culture medium enhances IL 1 production. Among serum factors, anaphylatoxins C3a and C5a and/or their desArg derivatives have been shown to enhance LPS-induced IL 1 and TNF production. However, the capacity of natural anaphylatoxins to induce by themselves the production of cytokines remains a controversial issue. We have investigated the capacity of human recombinant C5a (hrC5a) to induce IL 1 and TNF production. Despite its lack of direct triggering, hrC5a was able to act synergistically with LPS, leading to higher IL 1 and TNF release by human monocytes and mouse peritoneal macrophages. As assessed by the comitogenic assay, hrC5a increased IL 1 release, whereas cell-associated IL 1 activity was not significantly modified. Measurement by enzyme-linked immunosorbent assay of human IL 1.beta. led to similar conclusions, whereas measurement of IL 1.alpha. by radioimmunoassay indicated, in addition an increase in intracellular IL 1.alpha.