Relationship between ureB sequence diversity, urease activity and genotypic variations of different Helicobacter pylori strains in patients with gastric disorders

• Autorzy: Ghalehnoei H. , Ahmadzadeh A. , Farzi N. , Alebouyeh M. , Aghdaei H.A. , Azimzadeh P. , Molaei M. , Zali M.R.
• Języki publikacji: EN

Abstrakty

EN

Association of the severity of Helicobacter pylori induced diseases with virulence entity of the colonized strains was proven in some studies. Urease has been demonstrated as a potent virulence factor for H. pylori. The main aim of this study was investigation of the relationships of ureB sequence diversity, urease activity and virulence genotypes of different H. pylori strains with histopathological changes of gastric tissue in infected patients suffering from different gastric disorders. Analysis of the virulence genotypes in the isolated strains indicated significant associations between the presence of severe active gastritis and cagA⁺ (P = 0.039) or cagA/iceA1 genotypes (P = 0.026), and intestinal metaplasia and vacA m1 (P = 0.008) or vacA s1/m2 (P = 0.001) genotypes. Our results showed a 2.4-fold increased risk of peptic ulcer (95% CI: 0.483–11.93), compared with gastritis, in the infected patients who had dupA positive strains; however this association was not statistically significant. The results of urease activity showed a significant mean difference between the isolated strains from patients with PUD and NUD (P = 0.034). This activity was relatively higher among patients with intestinal metaplasia. Also a significant association was found between the lack of cagA and increased urease activity among the isolated strains (P = 0.036). While the greatest sequencevariation of ureB was detected in a strain from a patient with intestinal metaplasia, the sole determined amino acid change in UreB sequence (Ala201Thr, 30%), showed no influence on urease activity. In conclusion, the supposed role of H. pylori urease to form peptic ulcer and advancing of intestinal metaplasia was postulated in this study. Higher urease activity in the colonizing H. pylori strains that present specific virulence factors was indicated as a risk factor for promotion of histopathological changes of gastric tissue that advance gastric malignancy.

• Wydawca: -
• Czasopismo: Polish Journal of Microbiology
• Rocznik: 2016
• Tom: 65
• Numer: 2
• Opis fizyczny: p.153-159,fig.,ref.

Twórcy

autor

Ghalehnoei H.

• Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
• Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

autor

Ahmadzadeh A.

• Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
• Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

autor

Farzi N.

• Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

autor

Alebouyeh M.

• Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
• Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

autor

Aghdaei H.A.

• Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
• Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

autor

Azimzadeh P.

autor

Molaei M.

• Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

autor

Zali M.R.

• Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
• Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Bibliografia

• Arachchi H.S., V. Kalra, B. Lal, V. Bhatia, C.S. Baba, S. Chakravarthy, S. Rohatgi, S., P.M. Sarma, V. Mishra, B. Das and others. 2007. Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian Population. Helicobacter 12: 591–597.
• Argent R.H., A. Burette, V.Y. Miendje Deyi and J.C. Atherton. 2007. The presence of dupA in Helicobacter pylori is not significantly associated with duodenal ulceration in Belgium, South Africa, China, or North America. Clin. Infect. Dis. 45: 1204–1206.
• Argent R.H., R.J. Thomas, D.P. Letley, M.G. Rittig, K.R. Hardie and J.C. Atherton. 2008. Functional association between the Helicobacter pylori virulence factors VacA and CagA. J. Med. Microbiol. 57: 145–150.
• Atherton J.C. 1997. The clinical relevance of strain types of Helicobacter pylori. Gut. 40: 701–703.
• Aydin F., N. Kaklikkaya, O. Ozgur, K. Cubukcu, A.O. Kilic, I. Tosun and M. Erturk. 2004. Distribution of vacA alleles and cagA status of Helicobacter pylori in peptic ulcer disease and non-ulcer dyspepsia. Clin Microbiol. Infect. 10: 1102–1104.
• Benoit S.L., N. Mehta, M.V. Weinberg, C. Maier and R.J. Maier. 2007. Interaction between the Helicobacter pylori accessory proteins HypA and UreE is needed for urease maturation. Microbiology 153: 1474–1482.
• Beswick E.J., I.V. Pinchuk, K. Minch, G. Suarez, J.C. Sierra, Y. Yamaoka and V.E. Reyes. 2006. The Helicobacter pylori urease B subunit binds to CD74 on gastric epithelial cells and induces NF-kappaB activation and interleukin-8 production. Infect. Immun. 74: 1148–1155.
• D’Elios M.M., A. Amedei, A. Cappon, G. Del Prete and M. de Bernard. 2007. The neutrophil-activating protein of Helicobacter pylori (HP-NAP) as an immune modulating agent. FEMS Immunol. Med. Microbiol. 50: 157–164.
• Dixon M.F., R.M. Genta, J.H. Yardley and P. Correa. 1996. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am. J. Surg. Pathol. 20: 1161–1181.
• Eaton K.A., J.V. Gilbert, E.A. Joyce, A.E. Wanken, T. Thevenot, P. Baker, A. Plaut and A. Wright. 2002. In vivo complementation of ureB restores the ability of Helicobacter pylori to colonize. Infect. Immun. 70: 771–778.
• Evans D.G., D.M. Queiroz, E.N. Mendes and D.J.Jr. Evans. 1998. Helicobacter pylori cagA status and s and m alleles of vacA in isolates from individuals with a variety of Helicobacter pylori – associated gastric diseases. J. Clin. Microbiol. 36: 3435–3437.
• Fan X., H. Gunasena, Z. Cheng, R. Espejo, S.E. Crowe, P.B. Ernst and V.E. Reyes. 2000. Helicobacter pylori urease binds to class II MHC on gastric epithelial cells and induces their apoptosis. J. Immunol. 165: 1918–1924.
• Farzi N., T. Malekian, M. Alebouyeh, F. Vaziri and M.R. Zali. 2014. Genotype diversity and quasispecies development of Helicobacter pylori in a single host. Jpn. J. Infect. Dis. 68(3): 176–80.
• Fong Y.H., H.C. Wong, M.H. Yuen, P.H. Lau, Y.W. Chen and K.B. Wong. 2013. Structure of UreG/UreF/UreH complex reveals how urease accessory proteins facilitate maturation of Helicobacter pylori urease. PLoS Biol. 11: e1001678.
• Gobert A.P., B.D. Mersey, Y. Cheng, D.R. Blumberg, J.C. Newton and K.T. Wilson. 2002. Cutting edge: Urease release by Helicobacter pylori stimulates macrophage inducible nitric oxide synthase. J. Immunol. 168: 6002–6006.
• Hu L.T., P.A. Foxall, R. Russell and H.L. Mobley. 1992. Purification of recombinant Helicobacter pylori urease apoenzyme encoded by ureA and ureB. Infect. Immun. 60: 2657–2666.
• Igarashi M., Y. Kitada, H. Yoshiyama, A. Takagi, T. Miwa and Y. Koga. 2001. Ammonia as an accelerator of tumor necrosis factor alpha-induced apoptosis of gastric epithelial cells in Helicobacter pylori infection. Infect. Immun. 69: 816–821.
• Ito S., Y. Kohli, T. Kato, H. Murakita, Y. Ohotaki, M. Hirai, T. Azuma and M. Kuriyama. 1995. Differences in urease activity in live Helicobacter pylori cultured from patients with gastroduodenal diseases. Eur. J. Gastroenterol. Hepatol. 7(Suppl 1): S83–88.
• Jung S.W., M. Sugimoto, S. Shiota, D.Y. Graham and Y. Yamaoka. 2012. The intact dupA cluster is a more reliable Helicobacter pylori virulence marker than dupA alone. Infect. Immun. 80: 381–387.
• Kohda K., K. Tanaka, Y. Aiba, M. Yasuda, T. Miwa and Y. Koga. 1999. Role of apoptosis induced by Helicobacter pylori infection in the development of duodenal ulcer. Gut. 44: 456–462.
• Kusters J.G., A.H. van Vliet and E.J. Kuipers. 2006. Pathogenesis of Helicobacter pylori infection. Clin. Microbiol. Rev. 19: 449–490.
• Lee M.H., Y. Roussel, M. Wilks and S. Tabaqchali. 2001. Expression of Helicobacter pylori urease subunit B gene in Lactococcus lactis mg1363 and its use as a vaccine delivery system against Helicobacter pylori infection in mice. Vaccine 19: 3927–3935.
• Lu H., P.I. Hsu, D.Y. Graham and Y. Yamaoka. 2005. Duodenal ulcer promoting gene of Helicobacter pylori. Gastroenterology 128: 833–848.
• McGee D.J. and H.L. Mobley. 1999. Mechanisms of Helicobacter pylori infection: bacterial factors. Curr. Top Microbiol. Immunol. 241: 155–180.
• Mobley H.L., M.D. Island and R.P. Hausinger. 1995. Molecular biology of microbial ureases. Microbiol. Rev. 59: 451–480.
• Muller I., A. Medina-Selby, J.L. Palacios, P. Martinez, P. Opazo, E. Bruce, M. Mancilla, P. Valenzuela, A. Yudelevich and A. Venegas. 2002. Cloning and comparison of ten gene sequences of a chilean Helicobacter pylori strain with other Helicobacter pylori strains revealed higher variability for VacA and CagA virulence factors. Biol. Res. 35: 67–84.
• Nguyen L.T., T. Uchida, Y. Tsukamoto, A. Kuroda, T. Okimoto, M. Kodama, K. Murakami, T. Fujioka and M. Moriyama. 2010. Helicobacter pylori dupA gene is not associated with clinical outcomes in the Japanese population. Clin. Microbiol. Infect. 16: 1264–1269.
• Nishiya D., T. Shimoyama, S. Fukuda, T. Yoshimura, M. Tanaka and A. Munakata. 2000. Evaluation of the clinical relevance of the iceA1 gene in patients with Helicobacter pylori infection in Japan. Scand. J. Gastroenterol. 35: 36–39.
• Nogueira C., C. Figueiredo, F. Carneiro, A.T. Gomes, R. Barreira, P. Figueira, C. Salgado, L. Belo, A. Peixoto, J.C. Bravo and others. 2001. Helicobacter pylori genotypes may determine gastric histopathology. Am. J. Pathol. 158: 647–654.
• Onal Okyay T. and D. Frigi Rodrigues. 2013. High throughput colorimetric assay for rapid urease activity quantification. J. Microbiol. Methods. 95: 324–326.
• Plummer M., L.J. van Doorn, S. Franceschi, B. Kleter, F. Canzian, J. Vivas, G. Lopez, D. Colin, N. Munoz and I. Kato. 2007. Helicobacter pylori cytotoxin-associated genotype and gastric precancerous lesions. J. Natl. Cancer Inst. 99: 1328–1334.
• Rathbone M. and B. Rathbone. 2011. Helicobacter pylori and gastric cancer. Recent Results Cancer Res. 185: 83–97.
• Ribeiro M.L., A.P. Godoy, Y.H. Benvengo, S. Mendonca and J.Jr. Pedrazzoli. 2003. Clinical relevance of the cagA, vacA and iceA genotypes of Helicobacter pylori in Brazilian clinical isolates. FEMS Immunol. Med. Microbiol. 36: 181–185.
• Shimoyama T., S. Fukuda, Q. Liu, S. Nakaji, Y. Fukuda and K. Suga-wara. 2003. Helicobacter pylori water soluble surface proteins prime human neutrophils for enhanced production of reactive oxygen species and stimulate chemokine production. J. Clin. Pathol. 56: 348–351.
• Suzuki H., T. Hibi and B.J. Marshall. 2007. Helicobacter pylori: present status and future prospects in Japan. J. Gastroenterol. 42: 1–15.
• Wang M.-Y., C. Shao, J. Li, Y.-C. Yang, S.-B. Wang, J.-L. Hao, C.-M. Wu, X.-Z. Gao and S.-H. Shao. 2015. Helicobacter pylori with the intact dupA cluster is more virulent than the strains with the incomplete dupA cluster. Curr. Microbiol. 71(1): 16–23
• World Health Organization (WHO). 1994. Schistosomes, liver flukes and Helicobacter pylori. IARC Working Group on the evaluation of carcinogenic risks to humans. Lyon, 7–14 June 1994. IARC Monogr Eval Carcinog Risks Hum. 61: 1–241.
• Wu H., T. Nakano, E. Daikoku, C. Morita, T. Kohno, H.H. Lian and K. Sano. 2005. Intrabacterial proton-dependent CagA transport system in Helicobacter pylori. J. Med. Microbiol. 54: 1117–1125.
• Wu H., T. Nakano, Y. Matsuzaki, Y. Ooi, T. Kohno, S. Ishihara and K. Sano. 2014. A new type of intrabacterial nanotransportation system for VacA in Helicobacter pylori. Med. Mol. Morphol. 47: 224–232.
• Xu J.K., C.S. Goodwin, M. Cooper and J. Robinson. 1990. Intracellular vacuolization caused by the urease of Helicobacter pylori. J. Infect. Dis. 161: 1302–1304.
• Yahav J., A. Fradkin, B. Weisselberg, A. Diver-Haver, H. Shmuely and A. Jonas. 2000. Relevance of CagA positivity to clinical course of Helicobacter pylori infection in children. J. Clin. Microbiol. 38: 3534–3537.
• Zhang J.Y., T. Liu, H. Guo, X.F. Liu, Y. Zhuang, S. Yu, L. Chen, C. Wu, Z. Zhao, B. Tang and others. 2011. Induction of a Th17 cell response by Helicobacter pylori urease subunit B. Immunobiology 216: 803–810.

Identyfikatory

DOI

10.5604/17331331.1204761