Shear stress upregulates IL-1β secretion by Chlamydia pneumoniae- infected monocytes.

Shear stress upregulates IL-1β secretion by Chlamydia pneumoniae- infected monocytes.
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剪切应力上调肺炎衣原体感染的单核细胞的IL-1β分泌。

DOI:
10.1002/bit.25486
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发表时间:
2015-04
影响因子:
3.8
通讯作者:
Ramasubramanian, Anand K.
Ramasubramanian, Anand K.
中科院分区:
工程技术2区
文献类型:
--
作者:
Cheeniyil, Aswathi;Evani, Shankar J.;Dallo, Shatha F.;Ramasubramanian, Anand K.

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感染因子越来越多地参与慢性炎性疾病的发展和进展。一些证据表明,常见的细胞内呼吸道病原体,肺炎衣原体有助于动脉粥样硬化的既定危险因素,但确切的机制还不清楚。认为C.肺炎感染的单核细胞从肺移动到动脉粥样硬化病灶,在此期间,细胞由于血流而经历机械刺激。在这项工作中,我们的特点是生理水平的剪切应力对C。肺炎感染的人单核细胞在体外流动模型。我们发现,5 dyn/cm 2的剪切应力仅在感染的单核细胞中增强促炎细胞因子IL-1β的表达,而在未感染的单核细胞中不增强。我们还发现这种增强是由于剪切应力引起的IL-1β基因表达上调。我们的研究结果表明,机械转导是一个重要的,迄今尚未解决的,感染的炎症反应的决定因素。
Infectious agents are increasingly implicated in the development and progression of chronic inflammatory diseases. Several lines of evidence suggest that the common intracellular respiratory pathogen, Chlamydia pneumoniae contributes to the well-established risk factors of atherosclerosis but the exact mechanism is not well understood. It is believed that C. pneumoniae-infected monocytes travel from the lung to the atherosclerotic foci, during which the cells experience mechanical stimuli due to blood flow. In this work, we characterized the effect of physiological levels of shear stress on C. pneumoniae-infected human monocytes in an in vitro flow model. We found that a shear stress of 5 dyn/cm2 enhanced the expression of pro-inflammatory cytokine IL-1β only in infected, but not in uninfected, monocytes. We also found that this enhancement is due to the upregulation of IL-1β gene expression due to shear stress. Our results demonstrate that mechanotransduction is an important, heretofore unaddressed, determinant of inflammatory response to an infection.
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