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。慢性肺炎支原体感染已被认为是炎症的促进剂，可能导致血管病变。尽管肺炎衣原体基因组已完全测序，但这一信息尚未导致对感染和靶细胞激活机制的理解，也未导致对潜在衣原体毒力因子的鉴定。此外，对宿主细胞因子促进肺炎原体感染、细胞内生长和存活的作用知之甚少。在我们的项目中，我们将解决以下假设：1。肺炎球菌介导的内皮细胞激活是否依赖于小gtp结合蛋白和内皮MAP激酶的磷酸化，这是靶细胞中的两个关键信号转导途径？2. 宿主因子（rho蛋白、map -激酶）是否促进内皮细胞中肺炎原体的感染、存活和生长？我们期待在内皮细胞激活方面肺炎原体-内皮细胞相互作用的新发病概念，以及基于内皮细胞的肺炎原体存活，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.