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首页> 外文期刊>Infection and immunity >Expression of Chemokine Genes in Human Dermal Microvascular Endothelial Cell Lines Infected with Orientia tsutsugamushi
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Expression of Chemokine Genes in Human Dermal Microvascular Endothelial Cell Lines Infected with Orientia tsutsugamushi

机译：东方tsu虫感染的人皮肤微血管内皮细胞系趋化因子基因的表达

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摘要

Scrub typhus, caused by Orientia tsutsugamushi, is characterized by local as well as systemic inflammatory manifestations. The main pathologic change is focal or disseminated multiorgan vasculitis, which is caused by the destruction of endothelial cells and perivascular infiltration of leukocytes. We investigated the regulation of chemokine induction in transformed human dermal microvascular endothelial cells (HMEC-1) in response to O. tsutsugamushiinfection. The monocyte chemoattractant protein-1 (MCP-1) and interleukin 8 (IL-8) mRNAs were induced, and their levels showed a transitory peak at 3 and 6 h, respectively. The RANTES transcript was detected at 6 h after infection, with increased levels evident by 48 h. The induction of the MCP-1 and IL-8 genes was not blocked by cycloheximide, suggesting that de novo protein synthesis of host cell proteins is not required for their transcriptional activation. Heat- or UV-inactivated O. tsutsugamushi induced a similar extent of MCP-1 and IL-8 responses. The induction of MCP-1 and IL-8 transcripts in the endothelial cells by O. tsutsugamushiwas not blocked by the inhibitors of NF-κB. Furthermore, the activation of NF-κB was not detected in HMEC-1 stimulated withO. tsutsugamushi. These results demonstrate that heat-stable molecules of O. tsutsugamushi induce the MCP-1 and IL-8 genes and the induction of the chemokine genes may be mediated by an NF-κB independent mechanism. We also showed that another major transcription factor, activator protein-1 (AP-1), was up-regulated in HMEC-1 after O. tsutsugamushi infection. This suggests the possible involvement of AP-1 in the chemokine gene expression.
机译：由东方typ虫（Orientia tsutsugamushi）引起的灌木斑疹伤寒具有局部和全身性炎症表现。主要病理改变是局灶性或弥散性多器官血管炎，其由内皮细胞的破坏和白细胞的血管周浸润引起。我们调查了转化肌对人类皮肤微血管内皮细胞（HMEC-1）趋化因子诱导的调控。 gam虫感染。诱导单核细胞趋化蛋白-1（MCP-1）和白介素8（IL-8）mRNA，它们的水平分别在3 h和6 h出现一个短暂的峰值。感染后6 h检测到RANTES转录本，至48 h明显升高。 MCP-1和IL-8基因的诱导没有被环己酰亚胺阻断，表明宿主细胞蛋白的从头蛋白质合成不需要它们的转录激活。热灭活或紫外线灭活的 O。 gam虫诱导了类似程度的MCP-1和IL-8反应。通过 O在内皮细胞中诱导MCP-1和IL-8转录物。 tsutsugamushi 不受NF-κB抑制剂的阻断。此外，在用emO刺激的HMEC-1中未检测到NF-κB的活化。 tsutsugamushi 。这些结果证明了 O的热稳定分子。 gam虫诱导MCP-1和IL-8基因，而趋化因子基因的诱导可能是由NF-κB独立机制介导的。我们还显示， O后，HMEC-1中的另一个主要转录因子活化蛋白1（AP-1）被上调。 tsutsugamushi 感染。这表明AP-1可能参与趋化因子基因表达。

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