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C5a在脂多糖或白细胞介素-1诱导的白细胞介素-6产生中的作用。

The role of C5a in interleukin-6 production induced by lipopolysaccharide or interleukin-1.

作者信息

Montz H, Koch K C, Zierz R, Götze O

机构信息

Department of Immunology, University of Göttingen, Germany.

出版信息

Immunology. 1991 Nov;74(3):373-9.

PMID:1769685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1384627/
Abstract

We investigated the effects of recombinant C5a on interleukin-6 (IL-6) production by peripheral blood mononuclear cells (PBMC) in vitro and compared them with the release of interleukin-1 (IL-1) and tumour necrosis factor (TNF). In a virtually lipopolysaccharide (LPS)-free culture system, C5a by itself did not induce any significant IL-6 translation. The IL-6 release in response to low amounts of LPS (500 pg/ml) or IL-1 beta, however, was markedly increased by the complement fragment. This enhancement of IL-6 synthesis was dose-dependent, reached its optimum at 5.8 x 10(-9)M rC5a and occurred regardless of the presence of serum components. At the level of transcription C5a by itself did not induce IL-6 gene expression, but in the presence of low amounts of LPS the stimulation of monocytes with C5a yielded an increase in IL-6 mRNA. The transcription of IL-1 beta, however, can be induced by C5a alone. These data are interesting, since they indicate a different regulation of IL-1 beta and IL-6 by the complement fragment C5a. Furthermore, we could show that the C5a-mediated IL-6 production influenced the synthesis of IgG rather than IgM in vitro. These results may be relevant for an understanding of the potentiating role of C5a in cytokine-dependent disease processes.

摘要

我们研究了重组C5a对体外人外周血单个核细胞(PBMC)白细胞介素-6(IL-6)产生的影响,并将其与白细胞介素-1(IL-1)和肿瘤坏死因子(TNF)的释放进行比较。在几乎无脂多糖(LPS)的培养系统中,C5a本身不会诱导任何显著的IL-6翻译。然而,在低剂量LPS(500 pg/ml)或IL-1β刺激下,补体片段可显著增加IL-6的释放。IL-6合成的这种增强是剂量依赖性的,在5.8×10^(-9)M重组C5a(rC5a)时达到最佳,且不受血清成分的影响。在转录水平上,C5a本身不会诱导IL-6基因表达,但在低剂量LPS存在的情况下,用C5a刺激单核细胞会使IL-6 mRNA增加。然而,IL-1β的转录可由C5a单独诱导。这些数据很有趣,因为它们表明补体片段C5a对IL-1β和IL-6的调节不同。此外,我们还发现C5a介导的IL-6产生在体外影响IgG而非IgM的合成。这些结果可能有助于理解C5a在细胞因子依赖性疾病过程中的增强作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86d9/1384627/0665e57952eb/immunology00114-0010-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86d9/1384627/0665e57952eb/immunology00114-0010-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86d9/1384627/0665e57952eb/immunology00114-0010-a.jpg

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