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 Nilsson, C.
Right arrow Articles by Engstrand, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nilsson, C.
Right arrow Articles by Engstrand, L.

 Previous Article  |  Next Article 

Infection and Immunity, November 2003, p. 6573-6581, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6573-6581.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Correlation between cag Pathogenicity Island Composition and Helicobacter pylori-Associated Gastroduodenal Disease

Christina Nilsson,1,2 Anna Sillén,1 Lena Eriksson,1 Mona-Lisa Strand,1 Helena Enroth,3 Staffan Normark,2 Per Falk,4 and Lars Engstrand1,2*

Swedish Institute for Infectious Disease Control, Solna,1 Microbiology and Tumorbiology Center,2 Department of Medicine, Karolinska Institute, Stockholm,4 Clinical Microbiology Laboratory, Capio Diagnostik AB, Skövde, Sweden3

Received 7 October 2002/ Returned for modification 20 January 2003/ Accepted 26 June 2003

Helicobacter pylori infection is associated with a variety of outcomes ranging from seemingly asymptomatic coexistence to peptic ulcer disease and gastric cancer. The cag pathogenicity island (PAI) contains genes associated with a more aggressive phenotype and has been suggested to be a determinant of severe disease outcome. The cagA gene has served as a marker for the cag PAI. However, the presence of this single gene does not necessarily indicate the presence of a complete set of cag PAI genes. We have analyzed the composition of the cag PAI in 66 clinical isolates obtained from patients with duodenal ulcer, gastric cancer, and nonulcer dyspepsia. Hybridization of DNA to microarrays containing all the genes of the cag PAI showed that 76 and 9% of the strains contained all or none of the cag PAI genes, respectively. Partial deletions of the cag PAI were found in 10 isolates (15%), of which 3 were cagA negative. The ability to induce interleukin-8 (IL-8) production in AGS cells was correlated to the presence of a complete cag PAI. Strains carrying only parts of the island induced IL-8 at levels significantly lower than those induced by cag PAI-positive isolates. The presence of an intact cag PAI correlates with development of more severe pathology, and such strains were found more frequently in patients with severe gastroduodenal disease (odds ratio, 5.13; 95% confidence interval, 1.5 to 17.4). Partial deletions of the cag PAI appear to be sufficient to render the organism less pathogenic.

* Corresponding author. Mailing address: Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden. Phone: 46 8 457 24 15. Fax: 46 8 30 17 97. E-mail: lars.engstrand{at}smi.ki.se.

Editor: V. J. DiRita

Infection and Immunity, November 2003, p. 6573-6581, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6573-6581.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sgouras, D. N., Panayotopoulou, E. G., Papadakos, K., Martinez-Gonzalez, B., Roumbani, A., Panayiotou, J., vanVliet-Constantinidou, C., Mentis, A. F., Roma-Giannikou, E. (2009). CagA and VacA Polymorphisms Do Not Correlate with Severity of Histopathological Lesions in Helicobacter pylori-Infected Greek Children. J. Clin. Microbiol. 47: 2426-2434 [Abstract] [Full Text]  
  • Nguyen, L. T., Uchida, T., Murakami, K., Fujioka, T., Moriyama, M. (2008). Helicobacter pylori virulence and the diversity of gastric cancer in Asia. J Med Microbiol 57: 1445-1453 [Abstract] [Full Text]  
  • Skoglund, A., Bjorkholm, B., Nilsson, C., Andersson, A. F., Jernberg, C., Schirwitz, K., Enroth, C., Krabbe, M., Engstrand, L. (2007). Functional Analysis of the M.HpyAIV DNA Methyltransferase of Helicobacter pylori. J. Bacteriol. 189: 8914-8921 [Abstract] [Full Text]  
  • Reyes-Leon, A., Atherton, J. C., Argent, R. H., Puente, J. L., Torres, J. (2007). Heterogeneity in the Activity of Mexican Helicobacter pylori Strains in Gastric Epithelial Cells and Its Association with Diversity in the cagA Gene. Infect. Immun. 75: 3445-3454 [Abstract] [Full Text]  
  • Salama, N. R., Gonzalez-Valencia, G., Deatherage, B., Aviles-Jimenez, F., Atherton, J. C., Graham, D. Y., Torres, J. (2007). Genetic Analysis of Helicobacter pylori Strain Populations Colonizing the Stomach at Different Times Postinfection. J. Bacteriol. 189: 3834-3845 [Abstract] [Full Text]  
  • Matteo, M. J., Granados, G., Perez, C. V., Olmos, M., Sanchez, C., Catalano, M. (2007). Helicobacter pylori cag pathogenicity island genotype diversity within the gastric niche of a single host. J Med Microbiol 56: 664-669 [Abstract] [Full Text]  
  • Mitchell, P., Germain, C., Fiori, P. L., Khamri, W., Foster, G. R., Ghosh, S., Lechler, R. I., Bamford, K. B., Lombardi, G. (2007). Chronic Exposure to Helicobacter pylori Impairs Dendritic Cell Function and Inhibits Th1 Development. Infect. Immun. 75: 810-819 [Abstract] [Full Text]  
  • Mattar, R., Marques, S. B., Monteiro, M. d. S., dos Santos, A. F., Iriya, K., Carrilho, F. J. (2007). Helicobacter pylori cag pathogenicity island genes: clinical relevance for peptic ulcer disease development in Brazil. J Med Microbiol 56: 9-14 [Abstract] [Full Text]  
  • Algood, H. M. S., Cover, T. L. (2006). Helicobacter pylori Persistence: an Overview of Interactions between H. pylori and Host Immune Defenses. Clin. Microbiol. Rev. 19: 597-613 [Abstract] [Full Text]  
  • Argent, R. H., Zhang, Y., Atherton, J. C. (2005). Simple Method for Determination of the Number of Helicobacter pylori CagA Variable-Region EPIYA Tyrosine Phosphorylation Motifs by PCR. J. Clin. Microbiol. 43: 791-795 [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]  


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