1887

Abstract

pathogenicity island (PAI) integrity was investigated in isolates from multiple biopsies recovered from 40 patients in an attempt to determine the co-existence of a varying PAI-positive to PAI-negative ratio in a single host. Six biopsies were obtained from each patient during the same endoscopic session. PAI analysis included amplification of seven loci (, , , , , HP0527 and HP0524) and the left end of II (LEC). Absence of the island was confirmed by empty-site PCR. - RFLP and random amplified polymorphic DNA PCR were used for strain delineation. The number of biopsies with -positive culture ranged from three to six per patient and a total of 218 isolates were recovered. Mixed infection was only found in two patients. Nearly one-third of the 40 patients harboured isolates with an intact PAI in all niches, another third of the isolates were empty-site-positive in all niches, whilst the remaining third of the isolates had a disrupted PAI in all or at least one of the niches. Co-existence of variants of the same strain with different PAI genotypes was observed in one-quarter of patients. The variations in PAI genotype included co-existence of: diverse PAI deletions in different niches, variants with intact and with partially deleted islands, variants with empty-site-positive and with partially deleted PAIs, and variants with an intact PAI and with empty-site-positive. Half of the patients with different PAI genotypes harboured an intact PAI in at least one niche. Co-existence of diverse genotypes of putative virulence factors in a single host must be considered when drawing a correlation with clinical presentation.

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2007-05-01
2020-07-13
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References

  1. Akada J. K., Ogura K., Dailidiene D., Dailide G., Cheverud J. M., Berg D. E. 2003; Helicobacter pylori tissue tropism: mouse-colonizing strains can target different gastric niches. Microbiology 149:1901–1909 [CrossRef]
    [Google Scholar]
  2. Blaser M. J., Berg D. E. 2001; Helicobacter pylori genetic diversity and risk of human disease. J Clin Invest 107:767–773 [CrossRef]
    [Google Scholar]
  3. Carroll I. M., Ahmed N., Beesley S. M., Khan A. A., Ghousunnissa S., Morain C. A., Habibullah C. M., Smyth C. J. 2004; Microevolution between paired antral and paired antrum and corpus Helicobacter pylori isolates recovered from individual patients. J Med Microbiol 53:669–677 [CrossRef]
    [Google Scholar]
  4. Fischer W., Puls J., Buhrdorf R., Gebert B., Odenbreit S., Haas R. 2001; Systematic mutagenesis of the Helicobacter pylori cag pathogenicity island: essential genes for CagA translocation in host cells and induction of interleukin-8. Mol Microbiol 42:1337–1348
    [Google Scholar]
  5. Hatakeyama M. 2004; Oncogenic mechanisms of Helicobacter pylori cagA protein. Nat Rev Cancer 4:688–694 [CrossRef]
    [Google Scholar]
  6. Hsu P. I., Hwang I., Cittelly D., Lai K. H., El-Zimaity H. M., Gutierrez O., Kim J. G., Osato M. S., Graham D. Y., Yamaoka Y. 2002; Clinical presentation in relation to diversity within the Helicobacter pylori cag pathogenicity island. Am J Gastroenterol 97:2231–2238 [CrossRef]
    [Google Scholar]
  7. Ikenoue T., Maeda S., Gura K. O., Akanuma M., Mitsuno Y., Imai Y., Yoshida H., Shiratori Y., Omata M. 2001; Determination of Helicobacter pylori virulence by simple gene analysis of the cag pathogenicity island. Clin Diagn Lab Immunol 8:181–186
    [Google Scholar]
  8. Jenks P. J., Megraud F., Labigne A. 1998; Clinical outcome after infection with Helicobacter pylori does not appear to be reliably predicted by the presence of any of the genes of the cag pathogenicity island. Gut 43:752–758 [CrossRef]
    [Google Scholar]
  9. Kauser F., Khan A. A., Hussain M. A., Carroll I. M., Ahmad N., Tiwari S., Shouche Y., Das B., Alam M. & other authors 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 [CrossRef]
    [Google Scholar]
  10. Kawamura O., Murakami M., Araki O., Yamada T., Tomizawa S., Shimoyama Y., Minashi K., Maeda M., Kusano M., Mori M. 2003; Relationship between gastric disease and deletion of cag pathogenicity island genes of Helicobacter pylori in gastric juice. Dig Dis Sci 48:47–53 [CrossRef]
    [Google Scholar]
  11. Kersulyte D., Chalkauskas H., Berg D. E. 1999; Emergence of recombinant strains of Helicobacter pylori during human infection. Mol Microbiol 31:31–43 [CrossRef]
    [Google Scholar]
  12. Konno M., Fujii N., Yokota S., Sato K., Takahashi M., Sato K., Mino E., Sugiyama T. 2005; Five-year follow-up study of mother-to-child transmission of Helicobacter pylori infection detected by a random amplified polymorphic DNA fingerprinting method. J Clin Microbiol 43:2246–2250 [CrossRef]
    [Google Scholar]
  13. Leanza A. G., Matteo M. J., Crespo O., Antelo P., Olmos J., Catalano M. 2004; Genetic characterisation of Helicobacter pylori isolates from an Argentinean adult population based on cag pathogenicity island right-end motifs, lsp A- glm M polymorphism and ice A and vac A genotypes. Clin Microbiol Infect 10:811–819 [CrossRef]
    [Google Scholar]
  14. Marshall D. G., Dundon W. G., Beesley S. M., Smyth C. J. 1998; Helicobacter pylori – a conundrum of genetic diversity. Microbiology 144:2925–2939 [CrossRef]
    [Google Scholar]
  15. Mukhopadhyay A. K., Kersulyte D., Jeong J. Y., Datta S., Ito Y., Chowdhury A., Chowdhury S., Santra A., Bhattacharya S. K. & other authors 2000; Distinctiveness of genotypes of Helicobacter pylori in Calcutta, India. J Bacteriol 182:3219–3227 [CrossRef]
    [Google Scholar]
  16. Naumann M. 2005; Pathogenicity island-dependent effects of Helicobacter pylori on intracellular signal transduction in epithelial cells. Int J Med Microbiol 295:335–341 [CrossRef]
    [Google Scholar]
  17. 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 [CrossRef]
    [Google Scholar]
  18. Nishiya D., Shimoyama T., Yoshimura T., Tanaka M., Fukuda S., Munakata A. 2004; Genes inside the cag PAI of Helicobacter pylori are not associated with gastric cancer in Japan. Hepatogastroenterology 51:891–894
    [Google Scholar]
  19. Rohde M., Puls J., Buhrdorf R., Fischer W., Haas R. 2003; A novel sheathed surface organelle of the Helicobacter pylori cag type IV secretion system. Mol Microbiol 49:219–234 [CrossRef]
    [Google Scholar]
  20. Sheu S. M., Sheu B. S., Yang Li H. B. C., Chu T. C., Wu J. J. 2002; Presence of ice A1 but not cag A,cag C, cag E, cag F, cag N,cag T, or orf 13 genes of Helicobacter pylori is associated with more severe gastric inflammation in Taiwanese. J Formos Med Assoc 101:18–23
    [Google Scholar]
  21. Shibata W., Hirata Y., Yoshida H., Otsuka M., Hoshida Y., Ogura K., Maeda S., Ohmae T., Yanai A. & other authors 2005; NF- κ B and ERK-signaling pathways contribute to the gene expression induced by cag PAI-positive- Helicobacter pylori infection. World J Gastroenterol 21:6134–6143
    [Google Scholar]
  22. van Doorn L. J., Figueiredo C., Rossau R., Jannes G., van Asbroek M., Sousa J. C., Carneiro F., Quint W. G. 1998; Typing of Helicobacter pylori vac A gene and detection of cag A gene by PCR and reverse hybridization. J Clin Microbiol 36:1271–1276
    [Google Scholar]
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