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Projekt
Signaling cascades of the CagA protein to induce host actin cytoskeletal rearrangements during infection with Helicobacter pylori
Antragsteller
Professor Dr. Steffen Backert
Fachliche Zuordnung
Zellbiologie
Förderung
Förderung von 2003 bis 2010
Projektkennung
Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 5407843
Helicobacter pylori is known as an etiological agent of chronic gastritis, duodenal ulcer and gastric cancer. H.pylori is capable of circumventing host response mechanisms including nuclear and cytoskeletal changes in gastric epithelial cells and to resist phagocytosis by professional phagocytes. Although several bacterial virulence factors such as the cytotoxin VacA or the CagA effector protein encoded by a type IV secretion system in the cag pathogenicity island (CagPAI) have been identified, molecular mechanisms of infection and persistence of H. plyori in the gastric mucosa are largely unknown. With this project we would like to foster our understanding of mechanisms underlying actin-cytoskeletal rearrangements induced by H. pylori. In particular, we would like to investigate the role of Rho GTPases and the bacterial CagA protein in modulation of the actin cytoskeleton of both gastric epithelial cells. Our focus is on host cell responses depending on a functional type IV secretion system in the CagPAI. As the pathogenetic process of H. pylori induced gastric diseases also depend on the contribution of host components, we will place an emphasis on the analysis of infected target cell responses upon intracellular signal transduction events. This approach will allow us to reconstruct the sequence of events occurring at the pathogen-host cell interface and will enable us to point out key determinants of this process that could be sensitive to intervention.
DFG-Verfahren
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