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

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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.