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首页> 外文期刊>Infection and immunity >Chlamydia pneumoniae Infection of Human Endothelial Cells Induces Proliferation of Smooth Muscle Cells via an Endothelial Cell-Derived Soluble Factor(s)
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Chlamydia pneumoniae Infection of Human Endothelial Cells Induces Proliferation of Smooth Muscle Cells via an Endothelial Cell-Derived Soluble Factor(s)

机译：人内皮细胞肺炎衣原体感染通过内皮细胞衍生的可溶性因子诱导平滑肌细胞增殖

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An association of Chlamydia pneumoniae with atherosclerosis and coronary heart disease has been determined epidemiologically and by the detection of C. pneumoniaeorganisms in atherosclerotic lesions in both humans and animal models of atherosclerosis. Previously, it has been shown that C. pneumoniae is capable of replicating in cell types found within atheromatous lesions, viz., endothelial cells, smooth muscle cells (SMC), and macrophages, yet the role of C. pneumoniae in the pathogenesis of atherosclerosis has not been determined. Since intimal thickening is a hallmark of atherosclerosis, we investigated whether C. pneumoniae infection of human umbilical vein endothelial cells (HUVEC) could induce the expression of a soluble factor(s) with mitogenic potential for SMC by using [3H]thymidine incorporation and direct cell counting. Conditioned medium harvested from HUVEC infected with C. pneumoniae stimulated SMC replication in a time- and dose-dependent fashion. Infection studies using various multiplicities of infection (MOIs) ranging from 0.001 to 1 demonstrated a dose-dependent production of the soluble factor(s). At an MOI of 1, SMC stimulation indices were 8.4 (P < 0.01) and 12.2 (P < 0.01) for conditioned media harvested at 24 and 48 h, respectively. To determine whether viable C. pneumoniae was required for production of the soluble factor(s), HUVEC were infected with heat-inactivated C. pneumoniae or with viable organisms in the presence of chloramphenicol. Both treatments produced stimulation indices similar to those for liveC. pneumoniae in the absence of chloramphenicol (P > 0.05), indicating that the factor(s) was produced by HUVEC and not by C. pneumoniae and that signal transduction events following chlamydia endocytosis may be important in the production of a soluble factor(s). The ability of C. pneumoniae to elicit an endothelial cell-derived soluble factor(s) that stimulates SMC proliferation may be important in the pathogenesis of atherosclerosis.
机译：通过流行病学和检测 C，确定了肺炎衣原体与动脉粥样硬化和冠心病的关系。人类和动物动脉粥样硬化模型中动脉粥样硬化病变中的肺炎生物。以前，已经显示 C。肺炎能够在动脉粥样硬化病变中发现的细胞类型中复制，即内皮细胞，平滑肌细胞（SMC）和巨噬细胞，但 C的作用。肺炎在动脉粥样硬化的发病机理中尚未确定。由于内膜增厚是动脉粥样硬化的标志，因此我们调查了是否 C。 [ 3 H]胸苷掺入法和直接细胞计数法可检测人脐静脉内皮细胞（HUVEC）肺炎感染可诱导SMC产生有丝分裂潜力的可溶性因子的表达。从感染了 C的HUVEC收获的条件培养基。肺炎以时间和剂量依赖性方式刺激SMC复制。使用范围从0.001到1的多种感染复数（MOI）进行的感染研究表明，可溶性因子的剂量依赖性产生。 MOI为1时，在24和48 h收获的条件培养基的SMC刺激指数分别为8.4（ P <0.01）和12.2（ P <0.01）。确定是否可行。肺炎是产生可溶性因子所必需的，HUVEC感染了热灭活的 C。肺炎或存在氯霉素的活菌。两种处理产生的刺激指数均与活体C相似。在没有氯霉素的情况下出现肺炎（ P C产生的。肺炎和衣原体内吞后的信号转导事件可能对可溶性因子的产生很重要。 C的能力。肺炎引起内皮细胞源性可溶性因子刺激SMC增殖可能在动脉粥样硬化的发病中起重要作用。

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