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Bacteriology

Molecular Basis of Pathogenicity in Helicobacter pylori Clinical Isolates

Ivy Bastos Ramis, Tesiê Leopoldo Fonseca, Ernani Pinho de Moraes, Márcia Silveira Fernandes, Raul Mendoza-Sassi, Obirajara Rodrigues, Carlos Renan Varela Juliano, Carlos James Scaini, Pedro Eduardo Almeida da Silva
Ivy Bastos Ramis
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Tesiê Leopoldo Fonseca
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Ernani Pinho de Moraes
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Márcia Silveira Fernandes
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Raul Mendoza-Sassi
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Obirajara Rodrigues
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Carlos Renan Varela Juliano
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Carlos James Scaini
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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Pedro Eduardo Almeida da Silva
Laboratório de Biologia Molecular, Universidade Federal do Rio Grande, Rua General Osório, S/N, Rio Grande, RS, Brazil
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  • For correspondence: pedre@furg.com.br
DOI: 10.1128/JCM.00472-10
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ABSTRACT

This study identified pathogenicity genes in 40 Helicobacter pylori clinical isolates. The cagA, vacA, and iceA genes were detected in 65%, 97.5%, and 97.5% of the isolates, respectively. The cagA, iceA1, and vacAs1a/m1 genes were related to erosive gastritis, whereas the vacAs2/m2 and iceA2 genes were associated with enanthematous gastritis.

Helicobacter pylori is considered the major etiologic agent of chronic active gastritis, an essential catalyst in the emergence of peptic ulcer, and a risk factor for the development of gastric cancer (17). Studies indicate that the evolution of the infection depends in part on the expression of specific bacterial pathogenicity genes, such as cagA (cytotoxin-associated gene A), vacA (vacuolating cytotoxin), and iceA (induced by contact with epithelium) (2).

The cagA gene is considered to be a marker for the presence of a cagA pathogenicity island (8). The cagA-positive H. pylori strains increase interleukin-8 production and gastric inflammation (5). The vacA gene encodes a vacuolating cytotoxin able to induce the formation of cytoplasmic vacuoles in epithelial cells (11). This gene comprises two variable regions: the signal region, with two alleles, s1 (subtypes s1a, s1b, and s1c) and s2, and the middle region, with the alleles m1 and m2 (3, 28). In general, the s1/m1 strains produce large amounts of vacuolating cytotoxin, the s1/m2 strains produce moderate amounts, and the s2/m2 strains produce little or none (3). The iceA gene has two alleles: iceA1 and iceA2. The iceA1 allele is associated with peptic ulcer, and iceA2 is related to asymptomatic gastritis (24, 29).

This study analyzed the presence of cagA, vacA, and iceA genes in clinical isolates and correlated these findings with the endoscopic diagnosis. Forty isolates of H. pylori were obtained from biopsy specimens of the gastric antrum collected from dyspeptic patients admitted to the upper gastrointestinal endoscopic ward in the Hospital of the Federal University of Rio Grande, Rio Grande do Sul, Brazil. This study was approved by the ethics committee of our university. Informed consent was obtained from all patients.

After collection, the biopsy specimens were kept in brain heart infusion broth (Acumedia, United States) with 20% glycerol and refrigerated (4 to 8°C) for a maximum of 4 h (22). This broth was thereafter vortexed, and 200 μl was added to medium Columbia agar (Oxoid, United Kingdom), supplemented with 7% sheep blood and with a selective mixture for Helicobacter species isolation (Cefar, Brazil). The agar plates were incubated under microaerophilic conditions (5 to 15% O2 and 10% CO2) at 37°C for 4 to 10 days (14). The identification of H. pylori was performed using catalase, oxidase, and urease tests, microscopy, and ureA gene detection (12, 19).

The DNA extraction was performed after 48 h of bacterial growth. Colonies were collected and resuspended in 500 μl of 1× TE buffer. The suspension was centrifuged at 10,000 × g for 5 min, and the supernatant was thereafter discarded. The DNA from the clinical isolates was then extracted with DNAzol reagent (Invitrogen, United States) by the method of the manufacturer.

The presence of the ureA, cagA, vacA, and iceA genes in the isolates was investigated by PCR using the primers described previously (6, 10, 21, 31). The PCR was performed as described by Rota et al. (for the ureA and cagA genes) and by Benenson et al. (for the alleles of the vacA and iceA genes) (4, 27).

The statistical analysis was performed by using Fisher's exact test, a chi-squared test, and a chi-squared test for linear trend. P values of less than 0.05 were considered statistically significant.

The presence of the pathogenicity genes was studied in 40 clinical isolates of H. pylori. From those, 50% (20 of 40) were obtained from patients with endoscopic diagnosis of enanthematous gastritis and 50% (20 of 40) were obtained from patients with erosive gastritis.

The cagA gene was identified in 65% (26 of 40) of the isolates. This frequency is similar to that found in previous studies of cagA in Brazil (14, 16, 18). The vacA and iceA genes were detected in 97.5% (39 of 40) of the samples. The vacAs1b (43.6%) and vacAm2 (53.9%) alleles were the most frequently detected in the 39 isolates, as well as the iceA2 allele (71.8%). This is an expected result, because these alleles have been reported in other studies (7, 18, 26). Moreover, 12.8% of the isolates verified the presence of the m1 and m2 alleles of the vacA gene, and 5.1% of the isolates had both iceA alleles. The detection of more than one allele of the middle region of vacA, as well as the identification of both iceA alleles in the same isolate, suggests coinfection of two different strains of H. pylori. Cases of patients being infected with multiple strains of H. pylori are not uncommon, being more frequent in areas of high H. pylori prevalence (9, 15, 23).

The association between the cagA and vacA genes is described in Table 1. All cagA-positive isolates confirmed the presence of vacA. The combinations vacAs1a/m1, vacAs1b/m1, vacAs1a/m2, vacAs1b/m2, and vacAs1b/m1m2 were present mainly in cagA-positive samples. A statistically significant association was observed between cagA and vacA (P < 0.001).

The relationship of pathogenicity genes with gastric disorders is described in Table 2. The cagA gene and the combination vacAs1a/m1 were frequently detected in isolates from patients with erosive gastritis. Similar findings were reported by other authors (14, 20). These genes are directly related to the infiltration of polymorphonuclear cells, which causes severe epithelial damage. Already, the combination vacAs2/m2 was frequently observed in isolates from patients with enanthematous gastritis, a finding that suggests that such alleles are related to minor damage in gastric mucosa (1). However, a statistically significant difference was not found in the association between either cagA or vacA and the clinical manifestations. The iceA1 allele was detected in 66.7% of isolates from patients with erosive gastritis, while iceA2 was identified in 57.1% of isolates from patients with enanthematous gastritis. The iceA1 allele may be associated with a more severe form of gastritis because iceA1-positive strains produce more inflammation-inducing cytokines, such as interleukin-8, which are potent chemotactic factors that activate polymorphonuclear leukocytes that contribute to enhanced inflammatory responses (13, 30). This finding agrees with those of previous studies (24, 25). In this work, a statistically significant association was observed between iceA and the endoscopic diagnosis (P = 0.047).

Based on the data presented above, we conclude that the detection of cagA, vacA, and iceA genes allows an improved evaluation of the pathogenic potential from clinical isolates. In this study, the cagA gene, the combination vacAs1a/m1, and the iceA1 allele were related to erosive gastritis; similarly, the combination vacAs2/m2 and the iceA2 allele were related to an attenuated form of gastritis. Therefore, the genotyping of the microorganism appears to be a clinically relevant procedure and can contribute to the prognosis of H. pylori infection.

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TABLE 1.

Association between the cagA gene and the allelic combinations of the vacA gene in isolates of H. pylori

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TABLE 2.

Distribution of the cagA gene and of the vacA and iceA alleles in isolates of H. pylori deriving from patients with different clinical manifestations

FOOTNOTES

    • Received 5 March 2010.
    • Returned for modification 17 June 2010.
    • Accepted 27 July 2010.
  • Copyright © 2010 American Society for Microbiology

REFERENCES

  1. 1.↵
    Araya, J. C., L. Anabalón, I. Roa, M. Bravo, M. A. Villaseca, P. Guzmán, and J. C. Roa. 2004. Relación de la genotipificación de Helicobacter pylori con la forma e intensidad de la gastritis en población adulta portadora de patología gástrica benigna. Rev. Med. Chil. 132 : 1345-1354.
    OpenUrlPubMed
  2. 2.↵
    Arents, N. L. A., A. A. Van Zwet, J. C. Thijs, A. M. D. Kooistra-Smid, K. R. Van Slochteren, J. E. Degener, J. H. Kleibeuker, and L.-J. Van Doorn. 2001. The importance of vacA, cagA, and iceA genotypes of Helicobacter pylori infection in peptic ulcer disease and gastroesophageal reflux disease. Am. J. Gastroenterol. 96 : 2603-2608.
    OpenUrlCrossRefPubMedWeb of Science
  3. 3.↵
    Atherton, J. C., P. Cao, R. M. Peek, Jr., M. K. R. Tummuru, M. J. Blaser, and T. L. Cover. 1995. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori: association of specific vacA types with cytotoxin production and peptic ulceration. J. Biol. Chem. 270 : 17771-17777.
    OpenUrlAbstract/FREE Full Text
  4. 4.↵
    Benenson, S., D. Halle, B. Rudensky, J. Faber, Y. Schlesinger, D. Branski, N. Rabinowitz, and M. Wilschanski. 2002. Helicobacter pylori genotypes in Israeli children: the significance of geography. J. Pediatr. Gastroenterol. Nutr. 35 : 680-684.
    OpenUrlCrossRefPubMed
  5. 5.↵
    Blaser, M. J., G. I. Perez-Perez, H. Kleanthous, T. L. Cover, R. M. Peek, P. H. Chyou, G. N. Stemmermann, and A. Nomura. 1995. Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res. 55 : 2111-2115.
    OpenUrlAbstract/FREE Full Text
  6. 6.↵
    Bukanov, N. O., and D. E. Berg. 1994. Ordered cosmid library and high-resolution physical-genetic map of Helicobacter pylori strain NCTC 11638. Mol. Microbiol. 11 : 509-523.
    OpenUrlCrossRefPubMedWeb of Science
  7. 7.↵
    Caner, V., M. Yilmaz, N. Yonetci, S. Zencir, N. Karagenc, I. Kaleli, and H. Bagci. 2007. H. pylori iceA alleles are disease-specific virulence factors. World J. Gastroenterol. 13 : 2581-2585.
    OpenUrlPubMed
  8. 8.↵
    Censini, S., C. Lange, Z. Xiang, J. E. Crabtree, P. Ghiara, M. Borodovsky, R. Rappuoli, and A. Covacci. 1996. cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc. Natl. Acad. Sci. U. S. A. 93 : 14648-14653.
    OpenUrlAbstract/FREE Full Text
  9. 9.↵
    Chiarini, A., C. Cala, C. Bonura, A. Gullo, G. Giuliana, S. Peralta, F. D'Arpa, and A. Giammanco. 2009. Prevalence of virulence-associated genotypes of Helicobacter pylori and correlation with severity of gastric pathology in patients from western Sicily, Italy. Eur. J. Clin. Microbiol. 28 : 437-446.
    OpenUrlCrossRef
  10. 10.↵
    Clayton, C. L., H. Kleanthous, P. J. Coates, D. D. Morgan, and S. Tabaqchali. 1992. Sensitive detection of Helicobacter pylori by using polymerase chain reaction. J. Clin. Microbiol. 30 : 192-200.
    OpenUrlAbstract/FREE Full Text
  11. 11.↵
    Cover, T. L. 1996. The vacuolating cytotoxin of Helicobacter pylori. Mol. Microbiol. 20 : 241-246.
    OpenUrlCrossRefPubMedWeb of Science
  12. 12.↵
    Datta, S., S. Chattopadhyay, A. Chowdhury, A. Santra, D. R. Saha, T. Ramamurthy, S. K. Bhattacharya, D. E. Berg, G. B. Nair, and A. K. Mukhopadhyay. 2005. Diagnosis and genotyping of Helicobacter pylori by polymerase chain reaction of bacterial DNA from gastric juice. J. Gastroenterol. Hepatol. 20 : 1253-1259.
    OpenUrlCrossRefPubMed
  13. 13.↵
    Dunn, B. E., H. Cohen, and M. J. Blaser. 1997. Helicobacter pylori. Clin. Microbiol. Rev. 10 : 720-741.
    OpenUrlAbstract/FREE Full Text
  14. 14.↵
    Fonseca, T. L., E. P. Moraes, C. R. Juliano, A. M. Silva, C. J. Scaini, R. A. Mendoza-Sassi, and P. E. A. Silva. 2009. Detection of Helicobacter pylori by phenotypic and genotypic methods. Dig. Dis. Sci. 55 : 1643-1648.
    OpenUrlPubMed
  15. 15.↵
    Gatti, L. L., E. K. F. Souza, K. R. Leite, E. L. S. Bastos, L. R. Vicentini, L. C. Silva, M. A. C. Smith, and S. L. M. Payão. 2005. cagA vacA alleles and babA2 genotypes of Helicobacter pylori associated with gastric disease in Brazilian adult patients. Diagn. Microbiol. Infect. Dis. 51 : 231-235.
    OpenUrlCrossRefPubMed
  16. 16.↵
    Gatti, L. L., J. L. P. Módena, S. L. M. Payão, M. A. C. Smith, Y. Fukuhara, J. L. P. Módena, R. B. Oliveira, and M. Brocchi. 2006. Prevalence of Helicobacter pylori cagA, iceA and babA2 alleles in Brazilian patients with upper gastrointestinal diseases. Acta Trop. 100 : 232-240.
    OpenUrlCrossRefPubMed
  17. 17.↵
    Go, M. F. 2002. Review article: natural history and epidemiology of Helicobacter pylori infection. Aliment. Pharmacol. Ther. 16 : 3-15.
    OpenUrl
  18. 18.↵
    Godoy, A. P. O., M. L. Ribeiro, Y. H. B. Benvengo, L. Vitiello, M. C. B. Miranda, S. Mendonça, and J. Pedrazzoli, Jr. 2003. Analysis of antimicrobial susceptibility and virulence factors in Helicobacter pylori clinical isolates. BMC Gastroenterol. 3 : 20.
    OpenUrlCrossRefPubMed
  19. 19.↵
    Kullavanijaya, P., D. Thong-Ngam, O. Hanvivatvong, P. Nunthapisud, P. Tangkijvanich, and P. Suwanagool. 2004. Analysis of eight different methods for the detection of Helicobacter pylori infection in patients with dyspepsia. J. Gastroenterol. Hepatol. 19 : 1392-1396.
    OpenUrlCrossRefPubMed
  20. 20.↵
    Kumar, S., A. Kumar, and V. K. Dixit. 2008. Direct detection and analysis of vacA genotypes and cagA gene of Helicobacter pylori from gastric biopsies by a novel multiplex polymerase chain reaction assay. Diagn. Microbiol. Infect. Dis. 62 : 366-373.
    OpenUrlCrossRefPubMed
  21. 21.↵
    Mattar, R., A. F. Santos, J. N. Eisig, T. N. Rodrigues, F. M. Silva, R. M. Lupinacci, K. Iriya, and F. J. Carrilho. 2005. No correlation of babA2 with vacA and cagA genotypes of Helicobacter pylori and grading of gastritis from peptic ulcer disease patients in Brazil. Helicobacter 10 : 601-608.
    OpenUrlCrossRefPubMed
  22. 22.↵
    Mégraud, F., and P. Lehours. 2007. Helicobacter pylori detection and antimicrobial susceptibility testing. Clin. Microbiol. Rev. 20 : 280-322.
    OpenUrlAbstract/FREE Full Text
  23. 23.↵
    Módena, J. L. P., A. I. L. Sales, G. O. Acrani, R. Russo, M. A. V. Ribeiro, Y. Fukuhara, W. D. Silveira, J. L. P. Módena, R. B. Oliveira, and M. Brocchi. 2007. Association between Helicobacter pylori genotypes and gastric disorders in relation to the cag pathogenicity island. Diagn. Microbiol. Infect. Dis. 59 : 7-16.
    OpenUrlCrossRefPubMed
  24. 24.↵
    Peek, R. M., Jr., S. A. Thompson, J. P. Donahue, K. T. Tham, J. C. Atherton, M. J. Blaser, and G. G. Miller. 1998. Adherence to gastric epithelial cells induces expression of a Helicobacter pylori gene, iceA, that is associated with clinical outcome. Proc. Assoc. Am. Physicians 110 : 531-544.
    OpenUrlPubMedWeb of Science
  25. 25.↵
    Peek, R. M., Jr., L.-J. van Doorn, J. P. Donahue, K. T. Tham, C. Figueiredo, M. J. Blaser, and G. G. Miller. 2000. Quantitative detection of Helicobacter pylori gene expression in vivo and relationship to gastric pathology. Infect. Immun. 68 : 5488-5495.
    OpenUrlAbstract/FREE Full Text
  26. 26.↵
    Ribeiro, M. L., A. P. O. Godoy, Y. H. B. Benvengo, S. Mendonca, and J. Pedrazzoli, Jr. 2003. Clinical relevance of the cagA, vacA and iceA genotypes of Helicobacter pylori in Brazilian clinical isolates. FEMS Immunol. Med. Microbiol. 36 : 181-185.
    OpenUrlCrossRefPubMed
  27. 27.↵
    Rota, C. A., J. C. Pereira-Lima, C. Blaya, and N. B. Nardi. 2001. Consensus and variable region PCR analysis of Helicobacter pylori 3′ region of cagA gene in isolates from individuals with or without peptic ulcer. J. Clin. Microbiol. 39 : 606-612.
    OpenUrlAbstract/FREE Full Text
  28. 28.↵
    Van Doorn, L.-J., C. Figueiredo, R. Sanna, S. Pena, P. Midolo, E. K. W. Ng, J. C. Atherton, M. J. Blaser, and W. G. V. Quint. 1998. Expanding allelic diversity of Helicobacter pylori vacA. J. Clin. Microbiol. 36 : 2597-2603.
    OpenUrlAbstract/FREE Full Text
  29. 29.↵
    Van Doorn, L.-J., C. Figuereido, R. Sanna, A. Plaisier, P. Schneeberger, W. de Boer, and W. Quint. 1998. Clinical relevance of the cagA, vacA, and iceA status of Helicobacter pylori. Gastroenterology 115 : 58-66.
    OpenUrlCrossRefPubMedWeb of Science
  30. 30.↵
    Xu, Q., and M. J. Blaser. 2001. Promoters of the CATG-specific methyltransferase gene hpyIM differ between iceA1 and iceA2 Helicobacter pylori strains. J. Bacteriol. 183 : 3875-3884.
    OpenUrlAbstract/FREE Full Text
  31. 31.↵
    Yamaoka, Y., T. Kodama, O. Gutierrez, J. G. Kim, K. Kashima, and D. Y. Graham. 1999. Relationship between Helicobacter pylori iceA, cagA, and vacA status and clinical outcome: studies in four different countries. J. Clin. Microbiol. 37 : 2274-2279.
    OpenUrlAbstract/FREE Full Text
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Molecular Basis of Pathogenicity in Helicobacter pylori Clinical Isolates
Ivy Bastos Ramis, Tesiê Leopoldo Fonseca, Ernani Pinho de Moraes, Márcia Silveira Fernandes, Raul Mendoza-Sassi, Obirajara Rodrigues, Carlos Renan Varela Juliano, Carlos James Scaini, Pedro Eduardo Almeida da Silva
Journal of Clinical Microbiology Sep 2010, 48 (10) 3776-3778; DOI: 10.1128/JCM.00472-10

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Molecular Basis of Pathogenicity in Helicobacter pylori Clinical Isolates
Ivy Bastos Ramis, Tesiê Leopoldo Fonseca, Ernani Pinho de Moraes, Márcia Silveira Fernandes, Raul Mendoza-Sassi, Obirajara Rodrigues, Carlos Renan Varela Juliano, Carlos James Scaini, Pedro Eduardo Almeida da Silva
Journal of Clinical Microbiology Sep 2010, 48 (10) 3776-3778; DOI: 10.1128/JCM.00472-10
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KEYWORDS

Helicobacter Infections
Helicobacter pylori
virulence factors

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