Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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Advances in Clinical and Experimental Medicine

2007, vol. 16, nr 1, January-February, p. 29–33

Publication type: original article

Language: English

The prevalence of Helicobacter pylori vacA alleles in patients with chronic gastritis

Wystepowanie alleli genu vacA u osób chorych na przewlekłe zapalenie żoładka zakażonych Helicobacter pylori

Marzena Zalewska−Ziob1,, Andrzej Wiczkowski1,, Joanna Katarzyna Strzelczyk1,, Brygida Adamek1,, Katarzyna Gawron1,, Gizela Trapp1,, Aleksander Sieroń2,, Anna Gadowska−Cicha2,

1 Department of General Biology, Medical University of Silesia, Zabrze, Poland

2 Chair and Clinic of Internal Diseases, Angiology, and Physical Medicine, Medical University of Silesia, Bytom, Poland

Abstract

Background. Helicobacter pylori is involved in the pathogenesis of peptic ulcer disease and associated with gastric carcinoma. Several virulence factors of H. pylori, including urease (Ure), vacuolating cytotoxin (VacA), and cytotoxin−associated antigen (CagA), have been identified.
Objectives. This study focused on the detection of the H. pylori cytotoxin−associated gene A (cagA) and genotyping of the vacuolating cytotoxin gene (vacA).
Material and Methods. The presence of the cagA gene and the diversity of the gene encoding the vacuolating cytotoxin were analyzed using PCR. The material consisted of 47 human gastric mucosa antrum biopsies derived from H. pylori−infected individuals with chronic gastritis.
Results. The cagA gene was present in 65.96% of the H. pylori strains. The VacA s1a/m2 (36.17%) and s2/m2 (36.17%) types were the most common. The VacA s1b/m1 strain was found only in one case (2.13%). The prevalence of s1a/m1 H. pylori strains was 19.15% and of s1b/m2 6.38%.
Conclusion. Chronic H. pylori−induced gastritis seems to be most often associated with the s1a/m2 and s2/m2 vacA gene allele combinations.

Streszczenie

Wprowadzenie. Helicobacter pylori jest czynnikiem etiologicznym choroby wrzodowej żołądka, a jego obecność wiąże się z występowaniem raka żołądka. Zidentyfikowano kilka czynników wirulencji H. pylori, w tym: ureazę (Ure), cytotoksynę wakuolizującą (VacA) oraz białko CagA.
Cel pracy. Detekcja genu cagA oraz określenie genotypu genu vacA H. pylori.
Materiał i metody. Obecność genu cagA i zróżnicowanie genu kodującego cytotoksynę VacA analizowano metodą PCR. Materiałem badanym było 47 wycinków błony śluzowej okolicy odźwiernikowej żołądka pochodzących od osób z przewlekłym zapaleniem żołądka zakażonych H. pylori.
Wyniki. Obecność genu cagA stwierdzono w 65,96% szczepów H. pylori. Najczęściej występującymi odmianami genu vacA były subtypy: s1a/m2 (36,17%) i s2/m2 (36,17%). Szczep s1b/m1 zidentyfikowano tylko w jednym przypadku (2,13%). Częstość występowania szczepów H. pylori s1a/m1 wynosiła 19,15%, a s1b/m2 – 6,38%.
Wnioski. Przewlekłe zakażenie H. pylori powodujące zapalenie błony śluzowej żołądka wydaje się najczęściej powiązane z kombinacją s1a/m2 oraz s2/m2 alleli genu vacA.

Key words

Helicobacter pylori, cagA gene, vacA gene alleles, PCR

Słowa kluczowe

Helicobacter pylori, gen cagA, allele genu vacA, PCR

References (25)

  1. Ando T, Peek RM., Pride D, Levine SM, Takata T, Lee Y−C, Kusugami K, van der Ende A, Kuipers EJ, Kusters JG, Blaser MJ: Polymorphisms of Helicobacter pylori HP0638 reflect geographic origin and correlate with cagA status. J Clin Microbiol 2002, 40, 239–246.
  2. Wen S, Felley CP, Bouzourene H, Reimers M, Michetti P, Pan−Hammarström Q: Inflammatory gene profiles in gastric mucosa during Helicobacter pylori infection in humans. J Immunol 2004, 172, 2595–2602.
  3. Shimoyama T, Crabtree JE: Bacterial factors and immune pathogenesis in Helicobacter pylori infection. Gut 1998, 43 (suppl 1), S2–S5.
  4. Krishnamurthy P, Parlow M, Zitzer JB, Vakil NB, Mobley HLT, Levy M, Phadnis SH, Dunn BE: Helicobacter pylori containing only cytoplasmic urease is susceptible to acid. Infect Immunol 1998, 66, 5060–5066.
  5. Han S−R, Schneider T, Loos M, Bhakdi S, Maeurer MJ: One−step polymerase chain reaction−based typing of Helicobacter pylori vacA gene: association with gastric histopathology. Med Microbiol Immunol 1999, 188, 131–138.
  6. Yan J, Mao Y−F: Construction of a prokaryotic expression system of vacA gene and detection of vacA gene, VacA protein in Helicobacter pylori isolates and anti−VacA antibody in patients’ sera. World J Gastroenterol 2004, 10, 985–990.
  7. Marais A, Mendz GL, Hazell SL, Mégraud F: Metabolism and genetics of Helicobacter pylori: the genome era. Microbiol Mol Biol Rev 1999, 63, 642–674.
  8. Van Doorn L−J, Figueiredo C, Sanna R, Pena S, Midolo P, Ng EKW, Atherton JC, Blaser MJ, Quint WGV: Expanding allelic diversity of Helicobacter pylori vacA. J Clin Microbiol 1998, 36, 2597–2603.
  9. Dzierżanowska D, Murawska B, Patzer J, Gzyl A: Application of molecular techniques for diagnosis of Helicobacter pylori infections. Mikrobiol Med 1998, 2, 48–52.
  10. Van Doorn L−J, Figueiredo C, Mégraud F, Pena S, Midolo P, de Magalhães Queiroz DM, Carneiro F, Vanderborght B, Pegado MGF, Sanna R, de Boer W, Schneeberger P, Correa P, Ng EKW, Atherton J, Blaser MJ, Quint WGV: Geographic distribution of vacA allelic types of Helicobacter pylori. Gastroenterol 1999, 116, 823–830.
  11. Van Doorn L−J, Figueiredo C, Sanna R, Plaisier A, Schneeberger P, de BoerW, Quint W: Clinical relevance of the cagA, vacA, and iceA status of Helicobacter pylori. Gastroenterology 1998, 115, 58–66.
  12. Schmidt H, Hensel M: Pathogenicity islands in bacterial pathogenesis. Clin Microbiol Rev 2004, 17, 14–56.
  13. Atherton JC, Cao P, Peek RM Jr, Tumuru MKR, Blaser MJ, Cover TL: Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori – association of specific vacA types with cytotoxin production and peptic ulceration. J Biol Chem 1995, 270, 17771–17777.
  14. Han S−R, Schreiber H−J, Bhakdi S, Loos M, Maeurer M: VacA genotypes and genetic diversity in clinical isolates of Helicobacter pylori. Clin Diagn Lab Immunol 1998, 5, 139–145.
  15. Covacci A, Rappuoli R: PCR amplification of gene sequences from Helicobacter pylori strains. In: Helicobacter pylori: techniques for clinical diagnosis and basic research. Eds.: Lee A, Megraud F, Saunders, London 1996, 94–111.
  16. Miehlke S, Kibler K, Kim JG: Allelic variation in the cagA gene of Helicobacter pylori obtained from Korea compared to the United States. Am J Gastroenterol 1996, 91, 1322–1325.
  17. Atherton JC: The clinical relevance of strain types of Helicobacter pylori. Gut 1997, 40, 701–703.
  18. Parsonnet J, Friedman GD, Orentreich N, Vogelman H: Risk for gastric cancer in people with CagA positive or CagA negative Helicobacter pylori infection. Gut 1997, 40, 297–301.
  19. Ando T, Peek RM, Lee Y−C, Krishna U, Kusugami K, Blaser MJ: Host cell responses to genotypically similar Helicobacter pylori isolates from United States and Japan. Clin Diagn Lab Immunol 2002, 9, 167–175.
  20. Gzyl A, Augustynowicz E, Dzierżanowska D, Rożynek E, Dura W, Celińska−Cedro D, Berg DE: Genotypes of Helicobacter pylori in Polish Population. Acta Microbiol Pol 1999, 48, 261–275.
  21. Gerhard M, Lehn N, Neumayer N, Boren T, Rad R, Schepp W, Miehlke S, Classen M, Prinz C: Clinical relevance of the Helicobacter pylori gene for blood−group antigen−binding adhesin. Proc Natl Acad Sci USA 1999, 96, 12778–12783.
  22. Pan ZJ, Berg DE, van der Hulst RW, Su WW, Raudonikiense A, Xiao SD. Dankert J, Tytgat GN: Prevalence of vacuolating cytotoxin production and distribution of distinct vacA alleles in Helicobacter pylori from China. J Infect Dis 1998, 178, 220–226.
  23. Vinion−Dubiel AD, McClain MS, Cao P. Mernaugh RL, Cover TL: Antigenic Diversity among Helicobacter pylori Vacuolating Toxins. Infect Immun 2001, 69, 4329–4336.
  24. Atherton JC, Peek RMJr, Tham KT, Cover TL, Blaser MJ: Clinical and pathological importance of heterogeneity in vacA, the vacuolating cytotoxin gene of Helicobacter pylori. Gastroenterology 1997, 112, 92–99.
  25. Podzorski RP, Podzorski DS, Wuerth A, Tolia V: Analysis of the vacA, cagA, cagE, iceA, and babA2 genes in Helicobacter pylori from sixty−one pediatric patients from the Midwestern United States. Diagn Microbiol Infect Dis 2003, 46, 83–88.
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