Erscheinungsdatum: 28.09.2015, Medium: Taschenbuch, Einband: Kartoniert / Broschiert, Titel: Innate immune signalling, Titelzusatz: NF-kappaB activation in infections with Helicobacter pylori or Legionella pneumophila, Autor: Bartfeld, Sina, Verlag: Südwestdeutscher Verlag für Hochschulschriften AG Co. KG, Sprache: Deutsch, Rubrik: Biologie // Allgemeines, Lexika, Seiten: 112, Informationen: Paperback, Gewicht: 183 gr, Verkäufer: averdo
Helicobacter pylori VacA and Calcium Signalling in T-cells ab 59.9 € als Taschenbuch: How Helicobacter pylori evade immune response; An insight of VacA effects on intracellular calcium signalling in T-cells. Aus dem Bereich: Bücher, Wissenschaft, Biologie,
Helicobacter pylori VacA and Calcium Signalling in T-cells ab 59.9 EURO How Helicobacter pylori evade immune response; An insight of VacA effects on intracellular calcium signalling in T-cells
More than 50% of the world's population harbor Helicobacter pylori in their upper gastrointestinal tract. H. pylori persistently infects gastric mucosa and is associated with several diseases including peptic ulcer disease and gastric carcinoma. One of the most thoroughly studied virulence factors produced by H. pylori is the Vacuolating Cytotoxin A (VacA).The protein binds to the host cells and is internalized. Inside the host cells, it causes "vacuole"-like membrane vesicles in the cytoplasm of gastric epithelial cells. Besides vacuolation, VacA exerts various other effects on target cells. VacA also forms membrane-embedded pores at the inner-mitochondrial membrane, resulting in mitochondrial dysfunction by cytochrome c release and apoptosis induction. VacA suppresses nuclear translocation of nuclear factor of activated T-cells (NFAT) resulting in down regulation of interleukin-2 (IL2) gene transcription to efficiently block proliferation of T-cells. This book underlines the results showing involvement of VacA in the modulation of intracellular calcium signalling and therefore will provide new insights that are required to understand how VacA inhibits T-cell proliferation.
During infection the human body interacts intimately with the infectious pathogen. It is this interaction that determines disease outcome. Upon infection the protein NF-kappaB acts as a central signal transmitter of the innate immune system. This protein has two main functions: the activation of genes important for inflammation as well as those that secure survival of the cell. This dual role provides a mechanistic link between infections and cancer development, as seen during infection with the carcinogenic bacterium Helicobacter pylori. Bacteria that develop intracellularly, such as Legionella pneumophila, depend on the survival of the host cell and can thus benefit from NF-kappaB activation. But how is NF-kappaB activated in these infections? And how is the activation terminated? The author introduces us to NF-kappaB signalling and then analyses NF-kappaB activation during infections with H. pylori or L. pneumophila. She establishes a new test system for high-throughput screenings and identifies new cellular factors important in NF-kappaB activation and termination. The identification of these factors broadens our understanding of innate immune signalling.