Krüll M, Klucken A C, Wuppermann F N, Fuhrmann O, Magerl C, Seybold J, Hippenstiel S, Hegemann J H, Jantos C A, Suttorp N
Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany.
J Immunol. 1999 Apr 15;162(8):4834-41.
Chlamydia pneumoniae is an important respiratory pathogen. Recently, its presence has been demonstrated in atherosclerotic lesions. In this study, we characterized C. pneumoniae-mediated activation of endothelial cells and demonstrated an enhanced expression of endothelial adhesion molecules followed by subsequent rolling, adhesion, and transmigration of leukocytes (monocytes, granulocytes). These effects were blocked by mAbs against endothelial and/or leukocyte adhesion molecules (beta1 and beta2 integrins). Additionally, activation of different signal transduction pathways in C. pneumoniae-infected endothelial cells was shown: protein tyrosine phosphorylation, up-regulation of phosphorylated p42/p44 mitogen-activated protein kinase, and NF-kappaB activation/translocation occurred within 10-15 min. Increased mRNA and surface expression of E-selectin, ICAM-1, and VCAM-1 were noted within hours. Thus, C. pneumoniae triggers a cascade of events that could lead to endothelial activation, inflammation, and thrombosis, which in turn may result in or may promote atherosclerosis.
肺炎衣原体是一种重要的呼吸道病原体。最近，已在动脉粥样硬化病变中证实其存在。在本研究中，我们对肺炎衣原体介导的内皮细胞活化进行了表征，并证明内皮黏附分子表达增强，随后白细胞（单核细胞、粒细胞）发生滚动、黏附和迁移。这些效应被针对内皮和/或白细胞黏附分子（β1和β2整合素）的单克隆抗体所阻断。此外，还显示了肺炎衣原体感染的内皮细胞中不同信号转导途径的激活：蛋白酪氨酸磷酸化、磷酸化的p42/p44丝裂原活化蛋白激酶上调以及NF-κB激活/易位在10-15分钟内发生。数小时内观察到E-选择素、细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）的mRNA和表面表达增加。因此，肺炎衣原体引发了一系列事件，这些事件可能导致内皮细胞活化、炎症和血栓形成，进而可能导致或促进动脉粥样硬化。
