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首页> 外文期刊>Infection and immunity >Host Cell Cytokines Induced by Chlamydia pneumoniae Decrease the Expression of Interstitial Collagens and Fibronectin in Fibroblasts
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Host Cell Cytokines Induced by Chlamydia pneumoniae Decrease the Expression of Interstitial Collagens and Fibronectin in Fibroblasts

机译：肺炎衣原体诱导的宿主细胞因子降低成纤维细胞间质胶原和纤连蛋白的表达

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Chlamydia pneumoniae infection has been associated with chronic obstructive airway disease (COPD), asthma, and atherosclerosis. Inflammation and airway remodeling in asthma and COPD result in subepithelial fibrosis that is characterized by the deposition of interstitial collagens and fibronectin. The progression of atherosclerosis is also accompanied by an increased production of interstitial collagens in the intima. As shown by reverse transcription-PCR and immunoblotting, infection of human fibroblasts and smooth muscle cells by C. pneumoniae TW-183 downregulated the expression of type I and III collagen and fibronectin, whereas the level of type IV collagen remained unchanged. Conditioned medium from infected fibroblasts as well as epithelial WISH cells also reduced the expression of interstitial collagens and fibronectin in uninfected cells. In experiments using blocking antibodies, beta interferon was found to contribute to the inhibitory effects of conditioned medium collected from infected fibroblasts. In contrast, downregulation of matrix protein expression by conditioned medium from epithelial cells was caused by interleukin-1α, which was not secreted from fibroblasts following chlamydial infection. C. pneumoniae-mediated inhibition of collagen and fibronectin expression was diminished following transfection of fibroblasts with specific small interfering RNA targeting the transcription factor CCAAT/enhancer-binding protein β. The downregulation of interstitial collagens and fibronectin by the Chlamydia-induced host cell cytokine response may modulate tissue remodeling processes in airway diseases. In atherosclerosis the inhibition of collagen synthesis by C. pneumoniae infection may promote plaque vulnerability, thereby increasing the risk of plaque rupture.
机译：肺炎衣原体感染与慢性阻塞性气道疾病（COPD），哮喘和动脉粥样硬化有关。哮喘和COPD中的炎症和气道重塑导致上皮下纤维化，其特征在于间质胶原和纤连蛋白的沉积。动脉粥样硬化的进展还伴随着内膜间质胶原蛋白的产生增加。如反转录PCR和免疫印迹所示， C感染人成纤维细胞和平滑肌细胞。肺炎链球菌TW-183下调I型和III型胶原和纤连蛋白的表达，而IV型胶原的水平保持不变。来自感染的成纤维细胞以及上皮WISH细胞的条件培养基也降低了未感染细胞中间质胶原和纤连蛋白的表达。在使用封闭抗体的实验中，发现β干扰素有助于从感染的成纤维细胞中收集条件培养基的抑制作用。相反，白细胞介素-1α引起上皮细胞条件培养基基质蛋白表达的下调，而衣原体感染后成纤维细胞并未分泌白介素-1α。 C。用靶向转录因子CCAAT /增强子结合蛋白β的特定小干扰RNA转染成纤维细胞后，肺炎病毒介导的对胶原蛋白和纤连蛋白表达的抑制作用减弱。衣原体诱导的宿主细胞细胞因子反应下调间质胶原和纤连蛋白可能调节气道疾病的组织重塑过程。在动脉粥样硬化中， C对胶原蛋白合成的抑制作用。肺炎感染可能会促进斑块易损性，从而增加斑块破裂的风险。

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