This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ikenoue, T.
Right arrow Articles by Omata, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ikenoue, T.
Right arrow Articles by Omata, M.

 Previous Article  |  Next Article 

Clinical and Diagnostic Laboratory Immunology, January 2001, p. 181-186, Vol. 8, No. 1
1071-412X/01/$04.00+0   DOI: 10.1128/CDLI.8.1.181-186.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Determination of Helicobacter pylori Virulence by Simple Gene Analysis of the cag Pathogenicity Island

Tsuneo Ikenoue,* Shin Maeda, Keiji Ogura, Masao Akanuma, Yuzo Mitsuno, Yasuo Imai, Haruhiko Yoshida, Yasushi Shiratori, and Masao Omata

Department of Gastroenterology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

Received 10 May 2000/Returned for modification 4 August 2000/Accepted 20 September 2000

Nucleic acid amplification was performed for five loci in the cag pathogenicity island (PAI) of Helicobacter pylori (comprising cagA, the cagA promoter region, cagE, cagT, and the left end of cagII [LEC]), and gastric inflammation in patients was evaluated. Of 204 H. pylori isolates from Japanese patients (53 with peptic ulcer, 55 with gastric cancer, and 96 with chronic gastritis), 197 (96.6%) were positive for all five loci. Two isolates (1%) were negative for all five loci, and five isolates (2.4%) were positive for only cagA and LEC. These latter seven isolates were all from patients with mild chronic gastritis. Neutrophil infiltration in gastric mucosa was significantly milder in patients infected with partially or totally deleted-PAI strains than in those with intact-PAI strains. The cagE gene was a more accurate marker of an intact cag PAI than the cagA gene, and cagE seemed to be more useful in discriminating between H. pylori strains causing different rates of disease progression.

* Corresponding author. Mailing address: Department of Gastroenterology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Phone: 81-3-3815-5411 ext. 3070. Fax: 81-3-3814-0021. E-mail: ikenoue-2im{at}h.u-tokyo.ac.jp.

Clinical and Diagnostic Laboratory Immunology, January 2001, p. 181-186, Vol. 8, No. 1
1071-412X/01/$04.00+0   DOI: 10.1128/CDLI.8.1.181-186.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Prouzet-Mauleon, V., Hussain, M. A., Lamouliatte, H., Kauser, F., Megraud, F., Ahmed, N. (2005). Pathogen Evolution In Vivo: Genome Dynamics of Two Isolates Obtained 9 Years Apart from a Duodenal Ulcer Patient Infected with a Single Helicobacter pylori Strain. J. Clin. Microbiol. 43: 4237-4241 [Abstract] [Full Text]  
  • Wu, C.-C., Chou, P.-Y., Hu, C.-T., Liu, Z.-C., Lin, C.-Y., Tseng, Y.-H., Lin, N.-T. (2005). Clinical Relevance of the vacA, iceA, cagA, and flaA Genes of Helicobacter pylori Strains Isolated in Eastern Taiwan. J. Clin. Microbiol. 43: 2913-2915 [Abstract] [Full Text]  
  • Kauser, F., Hussain, M. A., Ahmed, I., Ahmad, N., Habeeb, A., Khan, A. A., Ahmed, N. (2005). Comparing Genomes of Helicobacter pylori Strains from the High-Altitude Desert of Ladakh, India. J. Clin. Microbiol. 43: 1538-1545 [Abstract] [Full Text]  
  • Kauser, F., Khan, A. A., Hussain, M. A., Carroll, I. M., Ahmad, N., Tiwari, S., Shouche, Y., Das, B., Alam, M., Ali, S. M., Habibullah, C. M., Sierra, R., Megraud, F., Sechi, L. A., Ahmed, N. (2004). The cag Pathogenicity Island of Helicobacter pylori Is Disrupted in the Majority of Patient Isolates from Different Human Populations. J. Clin. Microbiol. 42: 5302-5308 [Abstract] [Full Text]  
  • Nilsson, C., Sillen, A., Eriksson, L., Strand, M.-L., Enroth, H., Normark, S., Falk, P., Engstrand, L. (2003). Correlation between cag Pathogenicity Island Composition and Helicobacter pylori-Associated Gastroduodenal Disease. Infect. Immun. 71: 6573-6581 [Abstract] [Full Text]  
  • Tomasini, M. L., Zanussi, S., Sozzi, M., Tedeschi, R., Basaglia, G., De Paoli, P. (2003). Heterogeneity of cag Genotypes in Helicobacterpylori Isolates from Human Biopsy Specimens. J. Clin. Microbiol. 41: 976-980 [Abstract] [Full Text]  
  • Sumie, A., Yamashiro, T., Nakashima, K., Nasu, M., Watanabe, M., Nishizono, A. (2001). Comparison of Genomic Structures and Antigenic Reactivities of Orthologous 29-Kilodalton Outer Membrane Proteins of Helicobacter pylori. Infect. Immun. 69: 6846-6852 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»