tailieunhanh - Báo cáo khoa học: Role of the cag-pathogenicity island encoded type IV secretion system in Helicobacter pylori pathogenesis

Helicobacter pyloriis a very successful human-specific bacterium world-wide. Infections of the stomach with this pathogen can induce pathologies, including chronic gastritis, peptic ulcers and even gastric cancer. Highly , | ịFEBS Journal MINIREVIEW Role of the cag-pathogenicity island encoded type IV secretion system in Helicobacter pylori pathogenesis Nicole Tegtmeyer1 Silja Wessler2 and Steffen Backert1 3 1 Schoolof Biomolecular and BiomedicalSciences Science Center West Belfield Campus University College Dublin Ireland 2 Department of Molecular Biology Division of Microbiology Paris-Lodron University of Salzburg Austria 3 Institute for MedicalMicrobiology Otto von Guericke University Magdeburg Germany Keywords Helicobacter pylori signalling type IV secretion VirB5 VirB10 Correspondence S. Backert University College Dublin Belfield Campus Schoolof Biomolecular and Biomedical Science Science Center West Dublin-4 Ireland Fax 353 1 716 1183 Tel 353 1 716 2155 E-mail Received 14 November 2010 revised 11 January 2011 accepted 27 January 2011 doi Helicobacter pylori is a very successful human-specific bacterium worldwide. Infections of the stomach with this pathogen can induce pathologies including chronic gastritis peptic ulcers and even gastric cancer. Highly virulent H. pylori strains encode the cytotoxin-associated gene cag -pathoge-nicity island which expresses a type IV secretion system T4SS . This T4SS forms a syringe-like pilus structure for the injection of virulence factors such as the CagA effector protein into host target cells. This is achieved by a number of T4SS proteins including CagI CagL CagY and CagA which by itself binds the host cell integrin member p1 followed by delivery of CagA across the host cell membrane. A role of CagA interaction with phosphatidylserine has also been shown to be important for the injection process. After delivery CagA becomes phosphorylated by oncogenic tyrosine kinases and mimics a host cell factor for the activation or inactivation of some specific intracellular signalling pathways. We review recent progress aiming to characterize the CagA-dependent and CagA-independent signalling .