Clinical relevance of the cagA, tnpA and tnpB genes in Helicobacter pylori

BMC Gastroenterology

Johannes G Kusters³  Jaap A Wagenaar¹  Marc JM Bonten³  Ashraf Mohhabati Mobarez²  Amin Talebi Bezmin Abadi² 

[1] Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, Netherlands;Department of Medical Bacteriology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran;Department of Medical Microbiology, University Medical Center Utrecht, Heidelberglaan 100, Utrecht 3584 CX, The Netherlands

关键词: Virulence factor;    Duodenal ulcer;    Gastric cancer;    Disease association;    Helicobacter pylori;   

Others  :  855704
DOI  :  10.1186/1471-230X-14-33

 received in 2013-07-26, accepted in 2014-01-30,  发布年份 2014

【 摘 要 】

Background

Numerous proteins have been proposed as virulence factors for the gram negative gastric bacterium Helicobacter pylori but only for a few this has unequivocally been demonstrated. The aim of the current study was to evaluate the association of the putative virulence factors tnpA and tnpB (no cagA) with H. pylori associated gastroduodenal diseases.

Methods

A PCR based assay was used to determine the presence of the tnpA and tnpB genes, as well as of cagA, in 360H. pylori strains isolated from H. pylori infected patients.

Results

Of 360H. pylori culture positive patients (196 men, 164 women; average age 42.1 years (range 17–73), 95 had gastritis, 92 had gastric ulcers, 108 had duodenal ulcers, and 65 had gastric cancer. Using the gastritis group as a reference a significantly aberrant gene distribution was observed for the tnpA (Relative risk: 1.45; 95% CI 1.04-1.93), the cagA (Relative risk: 1.81; 95% CI 1.44-2.29), but not the tnpB gene in the gastric cancer group.

Conclusions

The increased incidence of the tnpA gene in gastric cancer patients suggests a role of the tnpA gene in the development of H. pylori induced gastric cancer.

【 授权许可】

   
2014 Abadi et al.; licensee BioMed Central Ltd.

【 参考文献 】

• [1]Basso D, Plebani M, Kusters JG: Pathogenesis of Helicobacter pylori infection. Helicobacter 2010, 15(Suppl 1):14-20.
• [2]Sheu BS, et al.: Helicobacter pylori colonization of the human gastric epithelium: a bug’s first step is a novel target for us. J Gastroenterol Hepatol 2010, 25(1):26-32.
• [3]Hussein NR: The association of dupA and Helicobacter pylori-related gastroduodenal diseases. Eur J Clin Microbiol Infect Dis 2010, 29(7):817-821.
• [4]Kusters JG, van Vliet AH, Kuipers EJ: Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006, 19(3):449-490.
• [5]Kuipers EJ, et al.: Review article: the development of atrophic gastritis–Helicobacter pylori and the effects of acid suppressive therapy. Aliment Pharmacol Ther 1995, 9(4):331-340.
• [6]Taghvaei T, et al.: Prevalence of horB gene among the Helicobacter pylori strains isolated from dyspeptic patients: first report from Iran. Intern Emerg Med 2012, 7(6):505-508.
• [7]Talebi Bezmin Abadi A, Ghasemzadeh A, Mohabati Mobarez A: Low frequency of cagA-positive Helicobacter pylori strains isolated from Iranian patients with MALT lymphoma. Intern Emerg Med 2013, 8(1):49-53.
• [8]Saito Y, et al.: Conversion of Helicobacter pylori CagA from senescence inducer to oncogenic driver through polarity-dependent regulation of p21. J Exp Med 2010, 207(10):2157-2174.
• [9]Pachathundikandi SK, Tegtmeyer N, Backert : Signal transduction of Helicobacter pylori during interaction with host cell protein receptors of epithelial and immune cells. S Gut Microbes 2013, 4(6):454-474.
• [10]Censini S, et al.: cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci U S A 1996, 93(25):14648-14653.
• [11]Mattar R, et al.: Helicobacter pylori cag pathogenicity island genes: clinical relevance for peptic ulcer disease development in Brazil. J Med Microbiol 2007, 56(Pt 1):9-14.
• [12]Malekzadeh R, Derakhshan MH, Malekzadeh Z: Gastric cancer in Iran: epidemiology and risk factors. Arch Iran Med 2009, 12(6):576-583.
• [13]Talebi Bezmin Abadi A, et al.: Antibiotic resistance of Helicobacter pylori in Mazandaran, North of Iran. Helicobacter 2010, 15((6):505-509.
• [14]Salehi Z, et al.: Helicobacter pylori cagA status and peptic ulcer disease in Iran. Dig Dis Sci 2009, 54(3):608-613.
• [15]Dixon MF, Genta RM, Yardley JH, Correa P: Classification and grading of gastritis. The updated Sydney system. International workshop on the histopathology of gastritis, Houston 1994. Am J Surg Pathol 1996, 20(10):1161-1181.
• [16]Espinoza MG, et al.: Detection of the glmM gene in Helicobacter pylori isolates with a novel primer by PCR. J Clin Microbiol 2011, 49(4):1650-1652.
• [17]Mattar R, et al.: Association of LEC and tnpA Helicobacter pylori genes with gastric cancer in a Brazilian population. Infect Agent Cancer 2010, 5:1. BioMed Central Full Text
• [18]Abadi AT, Taghvaei T, Wolfram L, Kusters JG: Infection with Helicobacter pylori strains lacking dupA is associated with an increased risk of gastric ulcer and gastric cancer development. Med Microbiol 2012, 61(Pt 1):23-30.
• [19]Kersulyte D, et al.: Sequence organization and insertion specificity of the novel chimeric ISHp609 transposable element of Helicobacter pylori. J Bacteriol 2004, 186(22):7521-7528.
• [20]Kidd M, Louw JA, Marks IN: Helicobacter pylori in Africa: observations on an ‘enigma within an enigma’. J Gastroenterol Hepatol 1999, 14(9):851-858.
• [21]Ahmad T, et al.: Prevalence of Helicobacter pylori pathogenicity-associated cagA and vacA genotypes among Pakistani dyspeptic patients. FEMS Immunol Med Microbiol 2009, 55(1):34-38.
• [22]Talebi Bezmin Abadi A, et al.: Helicobacter pylori homB, but not cagA, is associated with gastric cancer in Iran. J Clin Microbiol 2011, 49(9):3191-3197.
• [23]Talebi Bezmin Abadi A, et al.: High correlation of babA (2)-positive strains of Helicobacter pylori with the presence of gastric cancer. Intern Emerg Med 2013, 8:497-501.