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Journal of Clinical Microbiology, February 2005, p. 786-790, Vol. 43, No. 2
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.2.786-790.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Tyrosine Phosphorylation of CagA from Chinese Helicobacter pylori Isolates in AGS Gastric Epithelial Cells

Youli Zhang,1,{dagger} Richard H. Argent,2*,{dagger} Darren P. Letley,2 Rachael J. Thomas,2 and John C. Atherton2

Division of Gastroenterology, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China,1 Institute of Infection, Immunity, and Inflammation and Wolfson Digestive Diseases Centre, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom2

Received 20 July 2004/ Returned for modification 13 September 2004/ Accepted 18 October 2004

Helicobacter pylori strains possessing the cag pathogenicity island (PaI) are associated with the development of gastroduodenal diseases, including gastric cancer. cag PaI products induce the secretion of interleukin-8 (IL-8) from epithelial cells and facilitate the translocation of CagA into the cell cytosol. In East Asia, where the incidence of gastric cancer is high, most strains possess the cag PaI. To date, however, no cag PaI phenotypic data have been provided for strains isolated in mainland China. Here we used 31 Chinese strains to determine the genotypic and phenotypic status of the cag PaI. All strains possessed cagA and cagE, and we observed a variation in the length of cagA variable regions. Nucleotide sequencing of the cagA variable region revealed that CagA was of two types, a short "Western" form with two tyrosine phosphorylation sites and a longer "East Asian" form with three tyrosine phosphorylation sites. Coculture of strains with AGS epithelial cells showed that strains could induce IL-8 secretion from the cells and that CagA with three phosphorylation sites became more phosphorylated than that with two and could induce significantly (P < 0.001) more cells to elongate. We hypothesize that the preponderance of the more active East Asian form of cagA may underlie the high rate of gastric cancer in China.

* Corresponding author. Mailing address: Institute of Infection, Immunity and Inflammation, C Floor West Block, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH, United Kingdom. Phone: 44 115 924 9924, ext. 41063. Fax: 44 115 970 9923. E-mail: richard.argent{at}nottingham.ac.uk.

{dagger} Y.Z. and R.H.A. contributed equally to this work.

Journal of Clinical Microbiology, February 2005, p. 786-790, Vol. 43, No. 2
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.2.786-790.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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