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本文引用的文献

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Pathophysiologic basis of sepsis: considerations for future strategies of intervention.脓毒症的病理生理基础:对未来干预策略的思考
Crit Care Med. 2000 Sep;28(9 Suppl):S4-8. doi: 10.1097/00003246-200009001-00002.
2
Soluble CD14 enhances membrane CD14-mediated responses to peptidoglycan: structural requirements differ from those for responses to lipopolysaccharide.可溶性CD14增强膜CD14介导的对肽聚糖的反应:其结构要求与对脂多糖反应的结构要求不同。
Infect Immun. 2000 Sep;68(9):5254-60. doi: 10.1128/IAI.68.9.5254-5260.2000.
3
The biology of Toll-like receptors.Toll样受体的生物学
Cytokine Growth Factor Rev. 2000 Sep;11(3):219-32. doi: 10.1016/s1359-6101(00)00006-x.
4
The interleukin-1 receptor/Toll-like receptor superfamily: signal generators for pro-inflammatory interleukins and microbial products.白细胞介素-1受体/Toll样受体超家族:促炎性白细胞介素和微生物产物的信号发生器
J Leukoc Biol. 2000 Apr;67(4):508-14. doi: 10.1002/jlb.67.4.508.
5
Toll-like receptor 4 imparts ligand-specific recognition of bacterial lipopolysaccharide.Toll样受体4赋予对细菌脂多糖的配体特异性识别。
J Clin Invest. 2000 Feb;105(4):497-504. doi: 10.1172/JCI8541.
6
Soluble CD14-mediated cellular responses to lipopolysaccharide.可溶性CD14介导的细胞对脂多糖的反应。
Chem Immunol. 2000;74:108-21. doi: 10.1159/000058751.
7
Interactions of CD14 with components of gram-positive bacteria.CD14与革兰氏阳性菌成分的相互作用。
Chem Immunol. 2000;74:83-107. doi: 10.1159/000058761.
8
Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2.前沿:天然免疫系统对革兰氏阳性菌细胞壁成分的识别是通过Toll样受体2实现的。
J Immunol. 1999 Jul 1;163(1):1-5.
9
Peptidoglycan- and lipoteichoic acid-induced cell activation is mediated by toll-like receptor 2.肽聚糖和脂磷壁酸诱导的细胞活化由Toll样受体2介导。
J Biol Chem. 1999 Jun 18;274(25):17406-9. doi: 10.1074/jbc.274.25.17406.
10
On the role of T lymphocytes in stimulation of humoral immunity induced by peptidoglycan-monomer linked with zinc.关于T淋巴细胞在锌连接的肽聚糖单体诱导的体液免疫刺激中的作用
Int Arch Allergy Immunol. 1999 May;119(1):13-22. doi: 10.1159/000024170.

CD14在肽聚糖单体激活人单核细胞过程中的作用。

The involvement of CD14 in the activation of human monocytes by peptidoglycan monomers.

作者信息

Muhvić D, El-Samalouti V, Flad H D, Radosević-Stasić B, Rukavina D

机构信息

Department of Physiology and Immunology, Medical Faculty, University of Rijeka, Croatia.

出版信息

Mediators Inflamm. 2001 Jun;10(3):155-62. doi: 10.1080/09629350123956.

DOI:10.1080/09629350123956
PMID:11545252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1781699/
Abstract

BACKGROUND

Cell-wall components of Gram-positive and Gram-negative bacteria induce the production of cytokines in human peripheral blood mononuclear cells. These cytokines are the main mediators of local or systemic inflammatory reaction that can contribute to the development of innate immunity.

AIMS

This study was performed to analyze the involvement of CD14 molecule in the activation of human monocytes by peptidoglycan monomer (PGM) obtained by biosynthesis from culture fluid of penicillin-treated Brevibacterium divaricatum NRLL-2311.

METHODS

Cytokine release of interleukin (IL)-1, IL-6 and tumor necrosis factor-alpha from human monocytes via soluble CD14 (sCD14) or membrane-associated (mCD14) receptor using anti-CD14 monoclonal antibody (MEM-18) or lipid A structure (compound 406) was measured in bioassays.

RESULTS

The results demonstrated that PGM in the presence of human serum might induce the monokine release in a dose-dependent manner. The addition of sCD14 at physiologic concentrations enhanced the PGM-induced monokine release, while the monokine inducing capacity of PGM in the presence of sCD14 was inhibited by MEM-18. Effects of PGM were also blocked by glycolipid, compound 406, suggesting the involvement of binding structures similar to those for lipopolysaccharide.

CONCLUSION

Activation of human monocytes by PGM involves both forms of CD14 molecule, sCD14 and mCD14.

摘要

背景

革兰氏阳性菌和革兰氏阴性菌的细胞壁成分可诱导人外周血单核细胞产生细胞因子。这些细胞因子是局部或全身炎症反应的主要介质,可促进固有免疫的发展。

目的

本研究旨在分析CD14分子在由青霉素处理的分叉短杆菌NRLL-2311培养液经生物合成获得的肽聚糖单体(PGM)激活人单核细胞过程中的作用。

方法

在生物测定中,使用抗CD14单克隆抗体(MEM-18)或脂多糖A结构(化合物406),通过可溶性CD14(sCD14)或膜相关(mCD14)受体测量人单核细胞释放白细胞介素(IL)-1、IL-6和肿瘤坏死因子-α的细胞因子水平。

结果

结果表明,在人血清存在的情况下,PGM可能以剂量依赖的方式诱导单核因子释放。生理浓度的sCD14的添加增强了PGM诱导的单核因子释放,而在sCD14存在的情况下,PGM的单核因子诱导能力被MEM-18抑制。PGM的作用也被糖脂化合物406阻断,表明存在与脂多糖类似的结合结构。

结论

PGM对人单核细胞的激活涉及sCD14和mCD14这两种形式的CD14分子。