Bedeutung von Nod1/2 für die Endothelzellaktivierung durch Chlamydophila pneumoniae.

肺炎衣原体是一种广泛存在的呼吸道病原体。慢性肺炎衣原体感染被认为是炎症的促进剂，可能导致血管损伤。虽然肺炎衣原体的基因组已经完全测序，但这些信息还没有导致对感染机制和靶细胞激活的了解，也没有识别潜在的衣原体毒力因子。此外，有关促进肺炎衣原体感染、细胞内生长和存活的宿主细胞因子的作用也知之甚少。在我们的项目中，我们将解决以下假设：1.肺炎衣原体介导的内皮细胞激活是否依赖于靶细胞中两个关键的信号转导途径--小GTP结合蛋白和内皮MAP激酶的磷酸化？2.宿主因素(Rho蛋白、MAP-Kinase)是否促进肺炎衣原体在内皮细胞中的感染、存活和生长？我们期待肺炎衣原体与内皮细胞相互作用的新致病概念在内皮激活和基于内皮细胞的肺炎衣原体存活方面，这可能导致新的治疗策略。

Chlamydia pneumoniae is a widespread respiratory pathogen. Chronic C. pneumoniae infection has been suggested as a promoter of inflammation that may result in vascular lesions. Although the genome of C. pneumoniae has been sequenced completely this information has not led yet to an understanding of the mechanisms of infection and target cell activation nor to the identification of potential chlamydial virulence factors. In addition little is know about the contribution of host cell factors that promote infection, intracellular growth and survival of C. pneumoniae. In our project we will address the following hypotheses: 1. Is C. pneumoniae mediated endothelial cell activation dependent on small GTP-binding proteins and phosphorylation of endothelial MAP kinases, two key signal transduction pathways in target cells ? 2. Do host factors (Rho-proteins, MAP-kinases) promote infection, survival and growth of C. pneumoniae in endothelial cells? We expect new pathogenetic concepts of C. pneumoniae - endothelial cell interaction in terms of endothelial activation as well as endothelial cell-based C. pneumoniae survival which may lead to novel therapeutic strategies.