Araştırma Makalesi
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Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran

Yıl 2016, Cilt: 1 Sayı: 1, 10 - 13, 21.05.2016
https://doi.org/10.5455/jicm.5.20160514

Öz

Background: Helicobacter pylori genome encodes a
large number of virulence and adhesion factors that involved in bacterial
adhesion to host cells and exerts its virulence effect with CagA
secretion.  In this study, we aimed to
examine the relationships between babA2
and cagA genotype and presence of
gastric disorders in patients from Iran.



Material and Methods: The presence of H.
pylori
and selected genes (cagA and
babA2) were detected by PCR method
from the genomic DNA of 105 patients who had been diagnosed with gastric
disorders like chronic gastritis by endoscopic and histopathologic routes.



Results:
Presence of H. pylori (glmM gene) was detected in 85 out of 105
(80.9%) patients. According to our results cagA
gene was found in 66 out of 85 (77.6%) patients and babA2 gene was found in 80 out of 85 (94.1%) patient.



Conclusion: In
conclusion, the cagA and babA2 genotypes might be considered as
useful biomarkers for non-ulcer disease (NUD) patients and gastric disorders in
the geographic region of Iran and the presence of H. pylori strains with double-positive status is high clinical
relevance to H. pylori-associated
diseases.

Kaynakça

  • Marshall B, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984; 323, 1311-1315.
  • Mayerle J, den Hoed CM, Schurmann C, Stolk L, Homuth G, Peters MJ, Völzke H, et al. Identification of genetic loci associated with Helicobacter pylori serologic status. Jama 2013; 309, 1912-1920.
  • Shaw SJ, Chen Y, Zheng H, Fu H, Burlingame MA, Marquez S, Hardy DJ. Structure-Activity Relationships of 9-Substituted-9-Dihydroerythromycin-Based Motilin Agonists: Optimizing for Potency and Safety. J Med Chem 2009; 52, 6851-6859.
  • Blaser MJ. Helicobacter pylori and gastric diseases. BMJ 1998; 316, 1507-1510.
  • Ilver D, Arnqvist A, Ögren J, Frick IM, Kersulyte D, Incecik E, TBorén T. Helicobacter pylori adhesin binding fucosylated histo-blood group antigens revealed by retagging. Science 1998; 279, 373-377.
  • Pride DT, Meinersmann RJ, Blaser MJ. Allelic variation within Helicobacter pylori babA and babB. J Immunol Infect 2001; 1; 69:1160-71.
  • Hsu PI, Hwang IR, Cittelly D, Lai KH, El-Zimaity HM, Gutierrez O, et al. Clinical presentation in relation to diversity within the Helicobacter pylori cag pathogenicity island. Am J Gastroenterol 2002; 97: 2231-2238.
  • Aspholm-Hurtig M, Dailide G, Lahmann M, Kalia A, Ilver D, Roche N, et al. Functional adaptation of BabA, the H. pylori ABO blood group antigen binding adhesin. Science 2004; 23; 305: 519-522.
  • Pohl MA, Romero-Gallo J, Guruge JL, Doris BT, Gordon JI, Blaser MJ. Host-dependent Lewis (Le) antigen expression in Helicobacter pylori cells recovered from Leb-transgenic mice. J Exp Med 2009; 206: 3061-3072.
  • Da Costa DM, dos Santos Pereira E, Rabenhorst, SHB. What exists beyond cagA and vacA? Helicobacter pylori genes in gastric diseases. World J Gastroenterol 2015; 21, 10563-10572.
  • Chomvarin C, Namwat W, Chaicumpar K, Mairiang P, Sangchan A, Sripa B, Tor-Udom S, Vilaichone RK. Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA and babA2 genotypes in Thai dyspeptic patients. Int J Infect Dis 2008; 12: 30-36.
  • Azevedo M, Eriksson S, Mendes N, Serpa J, Figueiredo C, Resende LP, et al. Infection by Helicobacter pylori expressing the BabA adhesin is influenced by the secretor phenotype. J Pathol 2008; 215: 308-316.
  • Erzin Y, Koksal V, Altun S, Dobrucali A, Aslan M, Erdamar S, et al. Role of host interleukin 1β gene (IL-1B) and interleukin 1 receptor antagonist gene (IL-1RN) polymorphisms in clinical outcomes in Helicobacter pylori-positive Turkish patients with dyspepsia. J Gastroenterol 2008; 43: 705-710.
  • Gerhard M, Lehn N, Neumayer N, Borén T, Rad R, Schepp W, et al. Clinical relevance of the Helicobacter pylori gene for blood-group antigen-binding adhesin. Proc Natl Acad Sci 1999; 96: 12778-12783.
  • Sheu BS, Sheu SM, Yang HB, Huang AH, Wu JJ. Host gastric Lewis expression determines the bacterial density of Helicobacter pylori in babA2 genopositive infection. Gut 2003; 52: 927-932.
  • Roesler, B.M. and Zeitune, J.M.R. From Gastritis to Gastric Cancer: The Importance of Cag PAI of Helicobacter pylori on the Development of Early and Advanced Gastric Adenocarcinoma. Clin Cancer Res 2012; 224.
Yıl 2016, Cilt: 1 Sayı: 1, 10 - 13, 21.05.2016
https://doi.org/10.5455/jicm.5.20160514

Öz

Kaynakça

  • Marshall B, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984; 323, 1311-1315.
  • Mayerle J, den Hoed CM, Schurmann C, Stolk L, Homuth G, Peters MJ, Völzke H, et al. Identification of genetic loci associated with Helicobacter pylori serologic status. Jama 2013; 309, 1912-1920.
  • Shaw SJ, Chen Y, Zheng H, Fu H, Burlingame MA, Marquez S, Hardy DJ. Structure-Activity Relationships of 9-Substituted-9-Dihydroerythromycin-Based Motilin Agonists: Optimizing for Potency and Safety. J Med Chem 2009; 52, 6851-6859.
  • Blaser MJ. Helicobacter pylori and gastric diseases. BMJ 1998; 316, 1507-1510.
  • Ilver D, Arnqvist A, Ögren J, Frick IM, Kersulyte D, Incecik E, TBorén T. Helicobacter pylori adhesin binding fucosylated histo-blood group antigens revealed by retagging. Science 1998; 279, 373-377.
  • Pride DT, Meinersmann RJ, Blaser MJ. Allelic variation within Helicobacter pylori babA and babB. J Immunol Infect 2001; 1; 69:1160-71.
  • Hsu PI, Hwang IR, Cittelly D, Lai KH, El-Zimaity HM, Gutierrez O, et al. Clinical presentation in relation to diversity within the Helicobacter pylori cag pathogenicity island. Am J Gastroenterol 2002; 97: 2231-2238.
  • Aspholm-Hurtig M, Dailide G, Lahmann M, Kalia A, Ilver D, Roche N, et al. Functional adaptation of BabA, the H. pylori ABO blood group antigen binding adhesin. Science 2004; 23; 305: 519-522.
  • Pohl MA, Romero-Gallo J, Guruge JL, Doris BT, Gordon JI, Blaser MJ. Host-dependent Lewis (Le) antigen expression in Helicobacter pylori cells recovered from Leb-transgenic mice. J Exp Med 2009; 206: 3061-3072.
  • Da Costa DM, dos Santos Pereira E, Rabenhorst, SHB. What exists beyond cagA and vacA? Helicobacter pylori genes in gastric diseases. World J Gastroenterol 2015; 21, 10563-10572.
  • Chomvarin C, Namwat W, Chaicumpar K, Mairiang P, Sangchan A, Sripa B, Tor-Udom S, Vilaichone RK. Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA and babA2 genotypes in Thai dyspeptic patients. Int J Infect Dis 2008; 12: 30-36.
  • Azevedo M, Eriksson S, Mendes N, Serpa J, Figueiredo C, Resende LP, et al. Infection by Helicobacter pylori expressing the BabA adhesin is influenced by the secretor phenotype. J Pathol 2008; 215: 308-316.
  • Erzin Y, Koksal V, Altun S, Dobrucali A, Aslan M, Erdamar S, et al. Role of host interleukin 1β gene (IL-1B) and interleukin 1 receptor antagonist gene (IL-1RN) polymorphisms in clinical outcomes in Helicobacter pylori-positive Turkish patients with dyspepsia. J Gastroenterol 2008; 43: 705-710.
  • Gerhard M, Lehn N, Neumayer N, Borén T, Rad R, Schepp W, et al. Clinical relevance of the Helicobacter pylori gene for blood-group antigen-binding adhesin. Proc Natl Acad Sci 1999; 96: 12778-12783.
  • Sheu BS, Sheu SM, Yang HB, Huang AH, Wu JJ. Host gastric Lewis expression determines the bacterial density of Helicobacter pylori in babA2 genopositive infection. Gut 2003; 52: 927-932.
  • Roesler, B.M. and Zeitune, J.M.R. From Gastritis to Gastric Cancer: The Importance of Cag PAI of Helicobacter pylori on the Development of Early and Advanced Gastric Adenocarcinoma. Clin Cancer Res 2012; 224.
Toplam 16 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Klinik Tıp Bilimleri
Bölüm Araştırma Makaleleri
Yazarlar

Mahsa Esmaeillu Bu kişi benim

Yayımlanma Tarihi 21 Mayıs 2016
Yayımlandığı Sayı Yıl 2016 Cilt: 1 Sayı: 1

Kaynak Göster

APA Esmaeillu, M. (2016). Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran. Journal of Immunology and Clinical Microbiology, 1(1), 10-13. https://doi.org/10.5455/jicm.5.20160514
AMA Esmaeillu M. Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran. J Immunol Clin Microbiol. Haziran 2016;1(1):10-13. doi:10.5455/jicm.5.20160514
Chicago Esmaeillu, Mahsa. “Prevalence of CagA and BabA2 Positive Helicobacter Pylori Strains in Dyspeptic Patients in Iran”. Journal of Immunology and Clinical Microbiology 1, sy. 1 (Haziran 2016): 10-13. https://doi.org/10.5455/jicm.5.20160514.
EndNote Esmaeillu M (01 Haziran 2016) Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran. Journal of Immunology and Clinical Microbiology 1 1 10–13.
IEEE M. Esmaeillu, “Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran”, J Immunol Clin Microbiol, c. 1, sy. 1, ss. 10–13, 2016, doi: 10.5455/jicm.5.20160514.
ISNAD Esmaeillu, Mahsa. “Prevalence of CagA and BabA2 Positive Helicobacter Pylori Strains in Dyspeptic Patients in Iran”. Journal of Immunology and Clinical Microbiology 1/1 (Haziran 2016), 10-13. https://doi.org/10.5455/jicm.5.20160514.
JAMA Esmaeillu M. Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran. J Immunol Clin Microbiol. 2016;1:10–13.
MLA Esmaeillu, Mahsa. “Prevalence of CagA and BabA2 Positive Helicobacter Pylori Strains in Dyspeptic Patients in Iran”. Journal of Immunology and Clinical Microbiology, c. 1, sy. 1, 2016, ss. 10-13, doi:10.5455/jicm.5.20160514.
Vancouver Esmaeillu M. Prevalence of cagA and babA2 positive Helicobacter pylori strains in dyspeptic patients in Iran. J Immunol Clin Microbiol. 2016;1(1):10-3.

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