The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis

Cell Communication and Signaling

Review

Steffen Backert¹  Silja Wessler²  Gernot Posselt² 

[1] Department of Biology, Institute for Microbiology, Friedrich Alexander University Erlangen/Nuremberg, Erlangen, Germany;Division of Molecular Biology, Department of Microbiology, Paris-Lodron University, Salzburg, Austria;

关键词: Epidermal Growth Factor Receptor;    Focal Adhesion Kinase;    CagA;    Gastric Epithelial Cell;    Pylorus Strain;   

DOI  :  10.1186/1478-811X-11-77

 received in 2013-08-05, accepted in 2013-10-01,  发布年份 2013

来源: Springer

【 摘 要 】

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.

【 授权许可】

Unknown   
© Posselt et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.