Skip to main content
Erschienen in: Digestive Diseases and Sciences 3/2009

01.03.2009 | Original Article

Helicobacter pylori cagA Status and Peptic Ulcer Disease in Iran

verfasst von: Zivar Salehi, Mohammad Halimi Jelodar, Mehdi Rassa, Moheb Ahaki, Hamidreza Mollasalehi, Farhad Mashayekhi

Erschienen in: Digestive Diseases and Sciences | Ausgabe 3/2009

Einloggen, um Zugang zu erhalten

Abstract

Helicobacterpylori contributes to the development of peptic ulcers and atrophic gastritis. Furthermore, H.pylori strains carrying the cagA gene are more virulent than cagA-negative strains and are associated with the development of gastric adenocarcinoma. The cagA gene is a putative H. pylori virulence factor of unknown function. The aim of this study was to determine the prevalence of the cagA gene among H. pylori isolates and its relationship with peptic ulcer disease in 128 Iranian patients. A total of 107 (83.6%) samples were positive, including 40 (95%) of the 42 patients with duodenal ulcer, 43 (86%) of the 50 patients with gastric ulcer, and 24 (66.6%) of the 36 patients with gastritis. cagA was present in 32 (80%) of 40 strains from duodenal ulcer patients, 33 (77%) of 43 strains from gastric ulcer patients, and 11 (46%) of 24 from gastritis patients. We also attempted to investigate the subtypes of 3′ region of cagA gene in H. pylori strains isolated from Iranian patients and their relation to H. pylori-associated gastroduodenal diseases. The PCR product of cagA positive strains obtained with primer set CAG1/CAG2 differed in size, varying from 642 to 651 bp (subtype A) in 33 isolates to 756 bp (subtype B/D) in 13 isolates. This does not support the view that subtypes of the 3′ region of cagA gene in H. pylori isolated from Iran correlate with the clinical outcomes of H. pylori, but colonization with cagA positive strains was significantly higher among duodenal ulcer than gastritis patients in Iran.
Literatur
1.
Zurück zum Zitat Blaser MJ, Perez-Perez GI, Kleanthous H, Cover TL, Peek RM, Chyou PH et al (1995) Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res 55:2111–2115PubMed Blaser MJ, Perez-Perez GI, Kleanthous H, Cover TL, Peek RM, Chyou PH et al (1995) Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res 55:2111–2115PubMed
4.
Zurück zum Zitat Parsonnet J, Friedman GP, Vandersteen DP, Chang Y, Vogelman JH, Orentriech N et al (1991) Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med 325:1127–1131PubMed Parsonnet J, Friedman GP, Vandersteen DP, Chang Y, Vogelman JH, Orentriech N et al (1991) Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med 325:1127–1131PubMed
6.
Zurück zum Zitat Campbell S, Fraser A, Holliss B, Schmid JO, Toole PW (1997) Evidence for ethnic tropism of Helicobacter pylori. Infect Immun 65:3708–3712PubMed Campbell S, Fraser A, Holliss B, Schmid JO, Toole PW (1997) Evidence for ethnic tropism of Helicobacter pylori. Infect Immun 65:3708–3712PubMed
7.
Zurück zum Zitat Taylor DN, Blaser MJ (1991) The epidemiology of Helicobacter pylori infection. Epidemiol Rev 13:42–59PubMed Taylor DN, Blaser MJ (1991) The epidemiology of Helicobacter pylori infection. Epidemiol Rev 13:42–59PubMed
8.
Zurück zum Zitat Atherton JC, Cao P, Peek RM, Tummuru MKR, Blaser MJ, Cover TL (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. doi:10.1074/jbc.270.30.17771 PubMedCrossRef Atherton JC, Cao P, Peek RM, Tummuru MKR, Blaser MJ, Cover TL (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. doi:10.​1074/​jbc.​270.​30.​17771 PubMedCrossRef
10.
11.
Zurück zum Zitat Montecucco C, de Bernard M (2003) Molecular and cellular mechanisms of action of the vacuolating cytotoxin (VacA) and neutrophil activating protein (HP-NAP) virulence factors of Helicobacter pylori. Microbes Infect 5:715–721. doi:10.1016/S1286-4579(03)00124-2 PubMedCrossRef Montecucco C, de Bernard M (2003) Molecular and cellular mechanisms of action of the vacuolating cytotoxin (VacA) and neutrophil activating protein (HP-NAP) virulence factors of Helicobacter pylori. Microbes Infect 5:715–721. doi:10.​1016/​S1286-4579(03)00124-2 PubMedCrossRef
12.
Zurück zum Zitat Satin B, Del Giudice G, Bianca VD, Dusi S, Laudanna C, Tonello F et al (2000) The neutrophil activating protein (HP-NAP) of Helicobacter pylori is a protective antigen and a major virulence factor. J Exp Med 191:1467–1476. doi:10.1084/jem.191.9.1467 PubMedCrossRef Satin B, Del Giudice G, Bianca VD, Dusi S, Laudanna C, Tonello F et al (2000) The neutrophil activating protein (HP-NAP) of Helicobacter pylori is a protective antigen and a major virulence factor. J Exp Med 191:1467–1476. doi:10.​1084/​jem.​191.​9.​1467 PubMedCrossRef
13.
Zurück zum Zitat Yamaoka Y, Osato MS, Sepulveda AR, Gutierrez O, Figura N, Kim JG et al (2000) Molecular epidemiology of Helicobacter pylori: separation of H. pylori from East Asian and non-Asian countries. Epidemiol Infect 124:91–96. doi:10.1017/S0950268899003209 PubMedCrossRef Yamaoka Y, Osato MS, Sepulveda AR, Gutierrez O, Figura N, Kim JG et al (2000) Molecular epidemiology of Helicobacter pylori: separation of H. pylori from East Asian and non-Asian countries. Epidemiol Infect 124:91–96. doi:10.​1017/​S095026889900320​9 PubMedCrossRef
14.
Zurück zum Zitat Lu H, Hsu PI, Graham D, Yamaoka Y (2005) Duodenal ulcer promoting gene of Helicobacter pylori. Gastroenterology 128:833–848PubMedCrossRef Lu H, Hsu PI, Graham D, Yamaoka Y (2005) Duodenal ulcer promoting gene of Helicobacter pylori. Gastroenterology 128:833–848PubMedCrossRef
15.
Zurück zum Zitat Censini S, Lange C, Xiang Z, Crabtree JE, Ghiara P, Borodovsky M et al (1996) Cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci USA 93:14648–14653. doi:10.1073/pnas.93.25.14648 PubMedCrossRef Censini S, Lange C, Xiang Z, Crabtree JE, Ghiara P, Borodovsky M et al (1996) Cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci USA 93:14648–14653. doi:10.​1073/​pnas.​93.​25.​14648 PubMedCrossRef
16.
Zurück zum Zitat Oliveira MJ, Costa AC, Costa AM, Henriques L, Suriano G, Atherton JC et al (2006) Helicobacter pylori induces gastric epithelial cell invasion in a c-Met and type IV secretion system-dependent manner. Biol Chem 46:34888–34896 Oliveira MJ, Costa AC, Costa AM, Henriques L, Suriano G, Atherton JC et al (2006) Helicobacter pylori induces gastric epithelial cell invasion in a c-Met and type IV secretion system-dependent manner. Biol Chem 46:34888–34896
19.
20.
Zurück zum Zitat Covacci A, Censini S, Bugnoli M, Petracca R, Burroni D, Macchia G et al (1993) Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci USA 90:5791–5795. doi:10.1073/pnas.90.12.5791 PubMedCrossRef Covacci A, Censini S, Bugnoli M, Petracca R, Burroni D, Macchia G et al (1993) Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci USA 90:5791–5795. doi:10.​1073/​pnas.​90.​12.​5791 PubMedCrossRef
21.
Zurück zum Zitat Tummuru MKR, Cover TL, Blaser MJ (1993) Cloning and expression of a high molecular weight major antigen of Helicobacter pylori: evidence of linkage to cytotoxin production. Infect Immun 61:1799–1809PubMed Tummuru MKR, Cover TL, Blaser MJ (1993) Cloning and expression of a high molecular weight major antigen of Helicobacter pylori: evidence of linkage to cytotoxin production. Infect Immun 61:1799–1809PubMed
22.
Zurück zum Zitat Higashi H, Tsutsumi R, Fujita A, Yamazaki S, Asaka M, Azuma T et al (2002) Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites. Proc Natl Acad Sci USA 99:14428–14433. doi:10.1073/pnas.222375399 PubMedCrossRef Higashi H, Tsutsumi R, Fujita A, Yamazaki S, Asaka M, Azuma T et al (2002) Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites. Proc Natl Acad Sci USA 99:14428–14433. doi:10.​1073/​pnas.​222375399 PubMedCrossRef
23.
Zurück zum Zitat Rudi J, Kolb C, Maiwald M, Kuck D, Sieg A, Galle PR et al (1998) Diversity of Helicobacter pylori vacA and cagA genes and relationship to VacA and cagA protein expression, cytotoxin production, and associated diseases. J Clin Microbiol 36:944–948PubMed Rudi J, Kolb C, Maiwald M, Kuck D, Sieg A, Galle PR et al (1998) Diversity of Helicobacter pylori vacA and cagA genes and relationship to VacA and cagA protein expression, cytotoxin production, and associated diseases. J Clin Microbiol 36:944–948PubMed
24.
Zurück zum Zitat Yamaoka Y, Kodama T, Kashima K, Graham DY, Sepulveda AR (1998) Variants of the 3′ region of the cagA gene in Helicobacter pylori isolates from patients with different H pylori-associated diseases. J Clin Microbiol 36:2258–2263PubMed Yamaoka Y, Kodama T, Kashima K, Graham DY, Sepulveda AR (1998) Variants of the 3′ region of the cagA gene in Helicobacter pylori isolates from patients with different H pylori-associated diseases. J Clin Microbiol 36:2258–2263PubMed
25.
Zurück zum Zitat Kidd M, Lastovica AJ, Atherton JC, Louw JA (1999) Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa? Gut 45:499–502PubMed Kidd M, Lastovica AJ, Atherton JC, Louw JA (1999) Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa? Gut 45:499–502PubMed
26.
Zurück zum Zitat Azuma T, Yamakawa A, Yamazaki S, Fukuta K, Ohtani M, Ito Y et al (2002) Correlation between variation of the 3′ region of the cagA gene in Helicobacter pylori and disease outcome in Japan. J Infect Dis 186:1621–1630. doi:10.1086/345374 PubMedCrossRef Azuma T, Yamakawa A, Yamazaki S, Fukuta K, Ohtani M, Ito Y et al (2002) Correlation between variation of the 3′ region of the cagA gene in Helicobacter pylori and disease outcome in Japan. J Infect Dis 186:1621–1630. doi:10.​1086/​345374 PubMedCrossRef
27.
Zurück zum Zitat Montgomery EA, Martin DF, Peura DA (1988) Rapid diagnosis of Campylobacter pylori by Gram’s stain. Am J Clin Pathol 90:606–609PubMed Montgomery EA, Martin DF, Peura DA (1988) Rapid diagnosis of Campylobacter pylori by Gram’s stain. Am J Clin Pathol 90:606–609PubMed
29.
Zurück zum Zitat Marais A, Mendz GL, Hazell SL, Megraud F (1999) Metabolism and genetics of Helicobacter pylori: the genome era. Microbiol Mol Biol Rev 63:642–674PubMed Marais A, Mendz GL, Hazell SL, Megraud F (1999) Metabolism and genetics of Helicobacter pylori: the genome era. Microbiol Mol Biol Rev 63:642–674PubMed
32.
Zurück zum Zitat Mendall MA (1997) Transmission of Helicobacter pylori. Semin Gastrointest Dis 8:113–123PubMed Mendall MA (1997) Transmission of Helicobacter pylori. Semin Gastrointest Dis 8:113–123PubMed
34.
Zurück zum Zitat Maeda S, Ogura K, Yoshida H, Kanai F, Ikenoue T, Kato N et al (1998) Major virulence factors, vacA and cagA, are commonly positive in Helicobacter pylori isolates in Japan. Gut 42:338–343PubMedCrossRef Maeda S, Ogura K, Yoshida H, Kanai F, Ikenoue T, Kato N et al (1998) Major virulence factors, vacA and cagA, are commonly positive in Helicobacter pylori isolates in Japan. Gut 42:338–343PubMedCrossRef
35.
Zurück zum Zitat Miehlke S, Kibler K, Kim JG, Figura N, Small SM, Graham DY et al (1996) Allelic variation in the cagA gene of Helicobacter pylori obtained from Korea compared to the United States. Am J Gastroenterol 91:1322–1325PubMed Miehlke S, Kibler K, Kim JG, Figura N, Small SM, Graham DY et al (1996) Allelic variation in the cagA gene of Helicobacter pylori obtained from Korea compared to the United States. Am J Gastroenterol 91:1322–1325PubMed
36.
Zurück zum Zitat Pan ZJ, van der Hulst RW, Feller M, Xiao SD, Tytgat GN, Dankert J et al (1997) Equally high prevalences of infection with cagA-positive Helicobacter pylori in Chinese patients with peptic ulcer disease and those with chronic gastritis-associated dyspepsia. J Clin Microbiol 35:1344–1347PubMed Pan ZJ, van der Hulst RW, Feller M, Xiao SD, Tytgat GN, Dankert J et al (1997) Equally high prevalences of infection with cagA-positive Helicobacter pylori in Chinese patients with peptic ulcer disease and those with chronic gastritis-associated dyspepsia. J Clin Microbiol 35:1344–1347PubMed
37.
Zurück zum Zitat Shimoyama T, Fukuda S, Tanaka M, Mikami T, Saito Y, Munakata A (1997) High prevalence of the cagA-positive Helicobacter pylori strains in Japanese asymptomatic patients and gastric cancer patients. Scand J Gastroenterol 32:465–468. doi:10.3109/00365529709025082 PubMedCrossRef Shimoyama T, Fukuda S, Tanaka M, Mikami T, Saito Y, Munakata A (1997) High prevalence of the cagA-positive Helicobacter pylori strains in Japanese asymptomatic patients and gastric cancer patients. Scand J Gastroenterol 32:465–468. doi:10.​3109/​0036552970902508​2 PubMedCrossRef
38.
Zurück zum Zitat Anderson H, Löivukene K, Sillakivi T, Maaroos HI, Ustav M, Peetsalu A et al (2002) Association of cagA and vacA genotypes of Helicobacter pylori with gastric diseases in Estonia. J Clin Microbiol 40:293–300 Anderson H, Löivukene K, Sillakivi T, Maaroos HI, Ustav M, Peetsalu A et al (2002) Association of cagA and vacA genotypes of Helicobacter pylori with gastric diseases in Estonia. J Clin Microbiol 40:293–300
Metadaten
Titel
Helicobacter pylori cagA Status and Peptic Ulcer Disease in Iran
verfasst von
Zivar Salehi
Mohammad Halimi Jelodar
Mehdi Rassa
Moheb Ahaki
Hamidreza Mollasalehi
Farhad Mashayekhi
Publikationsdatum
01.03.2009
Verlag
Springer US
Erschienen in
Digestive Diseases and Sciences / Ausgabe 3/2009
Print ISSN: 0163-2116
Elektronische ISSN: 1573-2568
DOI
https://doi.org/10.1007/s10620-008-0378-8

Weitere Artikel der Ausgabe 3/2009

Digestive Diseases and Sciences 3/2009 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

„Jeder Fall von plötzlichem Tod muss obduziert werden!“

17.05.2024 Plötzlicher Herztod Nachrichten

Ein signifikanter Anteil der Fälle von plötzlichem Herztod ist genetisch bedingt. Um ihre Verwandten vor diesem Schicksal zu bewahren, sollten jüngere Personen, die plötzlich unerwartet versterben, ausnahmslos einer Autopsie unterzogen werden.

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

17.05.2024 Direkte orale Antikoagulanzien Nachrichten

Kommt es zu einer nichttraumatischen Hirnblutung, spielt es keine große Rolle, ob die Betroffenen zuvor direkt wirksame orale Antikoagulanzien oder Marcumar bekommen haben: Die Prognose ist ähnlich schlecht.

Schlechtere Vorhofflimmern-Prognose bei kleinem linken Ventrikel

17.05.2024 Vorhofflimmern Nachrichten

Nicht nur ein vergrößerter, sondern auch ein kleiner linker Ventrikel ist bei Vorhofflimmern mit einer erhöhten Komplikationsrate assoziiert. Der Zusammenhang besteht nach Daten aus China unabhängig von anderen Risikofaktoren.

Semaglutid bei Herzinsuffizienz: Wie erklärt sich die Wirksamkeit?

17.05.2024 Herzinsuffizienz Nachrichten

Bei adipösen Patienten mit Herzinsuffizienz des HFpEF-Phänotyps ist Semaglutid von symptomatischem Nutzen. Resultiert dieser Benefit allein aus der Gewichtsreduktion oder auch aus spezifischen Effekten auf die Herzinsuffizienz-Pathogenese? Eine neue Analyse gibt Aufschluss.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.