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Title
The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis
AuthorPosselt, Gernot ; Backert, Steffen ; Wessler, Silja
Published in
Cell Communication and Signaling, London, 2013, Vol. 11, Issue 77, page 1-13
PublishedBioMed Central, 2013
LanguageEnglish
Document typeJournal Article
ISSN1478-811X
URNurn:nbn:at:at-ubs:3-324 Persistent Identifier (URN)
DOI10.1186/1478-811X-11-77 
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 The work is publicly available
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Abstract (English)

Infections with the human pathogen Helicobacter pylori (H. pylori) can lead to severe gastric diseases ranging from chronic gastritis and ulceration to neoplastic changes in the stomach. Development and progress of H. pylori-associated disorders are determined by multifarious bacterial factors. Many of them interact directly with host cells or require specific receptors, while others enter the host cytoplasm to derail cellular functions. Several adhesins (e.g. BabA, SabA, AlpA/B, or OipA) establish close contact with the gastric epithelium as an important first step in persistent colonization. Soluble H. pylori factors (e.g. urease, VacA, or HtrA) have been suggested to alter cell survival and intercellular adhesions. Via a type IV secretion system (T4SS), H. pylori also translocates the effector cytotoxin-associated gene A (CagA) and peptidoglycan directly into the host cytoplasm, where cancer- and inflammation-associated signal transduction pathways can be deregulated. Through these manifold possibilities of interaction with host cells, H. pylori interferes with the complex signal transduction networks in its host and mediates a multi-step pathogenesis.