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首页> 外文期刊>Infection and immunity >Cytokine and adhesion molecule expression in human monocytes and endothelial cells stimulated with bacterial heat shock proteins.
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Cytokine and adhesion molecule expression in human monocytes and endothelial cells stimulated with bacterial heat shock proteins.

机译：细菌热激蛋白刺激人单核细胞和内皮细胞中细胞因子和粘附分子的表达。

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Bacterial heat shock proteins (HSPs) from Escherichia coli (GroES, GroEL, and DNAk) were tested for their ability to induce by themselves the expression and release of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and granulocyte-monocyte colony-stimulating factor (GM-CSF) by human monocytes and GM-CSF, IL-6, E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by human umbilical vein endothelial cells (HUVEC). Our study demonstrated that treatment of monocytes with DNAk increased IL-6, TNF-alpha, and GM-CSF release in a dose-dependent manner. The same effect was elicited by GroEL but at a lower rate. Treatment of HUVEC cultures with DNAk and GroEL also increased GM-CSF, IL-6, E-selectin, ICAM-1, and VCAM-1 release in a dose-dependent fashion. In any case, the greatest release was obtained by using DNAk and GroEL at a concentration of 1 microg/ml. DNAk and GroEL were also able to up-regulate the surface expression of E-selectin, ICAM-1, and VCAM-1. As detected by reverse transcription-PCR analysis, DNAk and GroEL also increased the steady-state levels of cytokines and adhesion molecules in human monocytes and endothelial cells. In our study GroES showed a significant activity only on the release, surface expression, and mRNA transcription of E-selectin. Adhesion molecule expression seems to be a direct effect of HSPs and not via cytokines. Furthermore, these effects are due to HSPs properties because they are inhibited by specific monoclonal antibodies. These findings support the potential role of HSPs in modulating cell interactions during immunological and inflammatory responses.
机译：测试了来自大肠杆菌（GroES，GroEL和DNAk）的细菌热休克蛋白（HSP）自身诱导白细胞介素6（IL-6），肿瘤坏死因子α（TNF-alpha）表达和释放的能力。 ，以及人类单核细胞和GM-CSF，IL-6，E-选择素，细胞间粘附分子1（ICAM-1）和血管细胞粘附分子1（VCAM）的粒细胞-单核细胞集落刺激因子（GM-CSF） -1）通过人脐静脉内皮细胞（HUVEC）。我们的研究表明，用DNAk治疗单核细胞会以剂量依赖性方式增加IL-6，TNF-α和GM-CSF的释放。 GroEL产生了相同的效果，但速率较低。用DNAk和GroEL处理HUVEC培养物也以剂量依赖性方式增加了GM-CSF，IL-6，E-选择素，ICAM-1和VCAM-1的释放。在任何情况下，通过使用浓度为1微克/毫升的DNAk和GroEL可获得最大的释放。 DNAk和GroEL还能够上调E-选择蛋白，ICAM-1和VCAM-1的表面表达。如通过逆转录PCR分析所检测，DNAk和GroEL还增加了人类单核细胞和内皮细胞中细胞因子和粘附分子的稳态水平。在我们的研究中，GroES仅在E-选择素的释放，表面表达和mRNA转录上显示出显着活性。粘附分子表达似乎是HSP的直接作用，而不是通过细胞因子。此外，这些作用归因于HSPs特性，因为它们被特定的单克隆抗体抑制。这些发现支持了HSP在免疫和炎症反应过程中调节细胞相互作用的潜在作用。

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