Articles

Association between efficient adhesion to HEp-2 cells and severity of gastritis in Helicobacter pylori strains isolated from children

Abstract

Background and objectives: Helicobacter pylori causes chronic gastritis, peptic ulceration, and is a risk factor for gastric cancer. More than half of the world`s population is infected with this pathogen, however the disease outcome varies. Among the virulence factors of H. pylori, specific adhesions to gastric epithelium may be an important step in the induction of active inflammation. H. pylori displays considerable genetic diversity attributed to genetic drift during long-term colonization. Heterogeneity of clinical-isolates has considerably impacted in understanding the role of each factor in infection outcome. However, genetic change may be more limited in the stomach of children in the short period after infection. This work evaluates differences in adherence potential of strains isolated from children with various chronic- inflammation status.
Materials and Methods: A total of 157 children admitted to Medical Center of Tehran for upper gastrointestinal problems underwent endoscopy for H. pylori infection. Histological examination of their biopsies was performed after H& E and Giemsa staining. Gastritis and inflammation were graded according to the updated Sydney system. 70 culture-positive children, 20 were selected according to their histopathological status. Adherence of their H. pylori isolates to HEp- 2 cells was evaluated by viable count of bacteria associated with host cells in an optimized procedure developed in this study.
Results: Correlation was seen between inflammation severity score and efficiency of adhesion to HEp-2 cells. This correlation was not observed in the KB cell line as an epithelial cell-model.
Conclusion: Specific interaction of H. pylori with host gastric epithelium may be associated with disease outcome

Kikuchi S, and Dore P. 2005. Epidemiology of Helicobacter pylori Infection. Helicobacter. 10 (Suppl1):1-4.

Kusters JG, Van Vliet AHM, and Kuipers EJ.2006. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev. 19(3):449-490.

Penta R, De Falco M, Iaquinto G, De Luca A. Helicobacter pylori and gastric epithelial cells : from gastritis to cancer. J Exp Clin Cancer Res 2005; 24(3):337-45.

Warburton, S. E., N. P. Mapstone, A. T. R. Axon, P. Hawkey, M. F. Dixon. 1998. Clinical and Histological association of cagA and vacA in Helicobacter pylori gastritis. J Clin Pathol. 51:55-61.

Backert S, Schwarz T, Miehlke S, Kirsch C, Sommer C, Kwok T, et al. Functional analysis of the cag pathogenecity island in Helicobacter pylori isolates from Patients with gastritis, peptic ulcer, and gastric cancer. Infect Immun 2004; 72(2):1043-1056.

Nilsson C, Sillen A, Ericksson L, Strand ML, Enroth H, Normark S, Falk P, and Engstrand L. Correlation between cag pathogenecity island composition and Helicobacter pylori Associated Gastroduodenal Disease. Infect Immun 2003; 71(11):6573-6581.

Beckhed F, Torstensson E, Seguin D, Richter-Dahlfor A, and Rokbi B. Helicobacter pylori Infection induce Interleukin-8 receptor expression in the human gastric epithelium. Infect Immun 2003; 71(6):3357-3360.

Aspholm M, Kalia A, Ruhl S, Arnqvist A, et al. Helicobacter pylori Adhesion to carbohydrates. Methods Enzymol 2006; 417:293-339.

Aspholm-Hurtig M, Dailide G, Lahmann M, Kaalia A, Ilver D, Roche N, et al. Functional adaptation of BabA, the H. pylori ABO blood group antigen binding adhesin. Science 2004; 305(5683):519-22.

Yamaoka, Y., S. Kikuchi, H. M. el-Zimaity, O. Gutierrez, M. S. Osato, and D. Y. Graham. Importance of Helicobacter pylori oipA in clinical presentation, gastric inflammation, and mucosal interleukin 8 production. Gastroenterology 2002; 123:414–424.

Asphom M, Olfat FO, Norden J, Sonden B, et al. SabA is the H. pylori Hemagglutinin and is Polymorphic in Binding to Sialylated Glycans. PLoS Pathogens 2006;2(10):989-1001.

Mahdavi J, Sonden B, Hurtig M, Olfat FO, Forsberg L, Roche N, et al. Helicobacter pylori SabA adhesion in persistant infection and chronic inflammation. Science 2002; 297(5581):573-8.

Dixon MF, Genta RM, Yardley JH, and Gorrea P. Classification and grading of gastritis: the updated Sydney System. International workshop on the histopathology of gastritis, Houston, Texas. Am J Surg Pathol 1994; 20:1161-1181.

Israel DA, Salama N, Krishna KU, Rieger UM, Atherton JC, Falkow S, and Peek Jr RM. Helicobacter pylori genetic diversity within the gastric niche of a single human host. P N A S 2001; 98(25):14625-29.

Suerbaum S, Smith JM, Bapumia K, Morelli G, Smith N, Kunstmann E, Dyrek I, and Achtman M. Free recombination within Helicobacter pylori. P N A S 1998;95:12619-12624.

Smeets LC, Arents NLA, van Zwet AA, Vandenbroucke- Grauls CMJE, T. Verboom T, Bitter W, and Kusters JG. Molecular patchwork: chromosomal recombination between two Helicobacter pylori Strains during Natural Colonization. Infect Immun 2003;71(5):2907-2910.

Israel DA, Salama N, Arnold, CN, Moss SF, Ando T, Wirth HP, et al. Helicobacter pylori strain-specific difference in genetic content, identified by microarray, influence host inflammatory responses. J Clin Invest 2001;107(5):611-620. 26.

Falsafi T, Valizadeh N, Sepehr S, Najafi M. Application of a stool antigen test to evaluate the incidence of Helicobacter pylori infection in children and adolescents from Tehran, Iran. Clin Diagnost Lab Immunol 2005;9:1094-1097.

Alhomsi, M. F; and E. O. Adeyemi. Grading Helicobacter pylori gastritis in dyspeptic patients. Comp Immun Microbiol Infect Dis 1996; 19(2):147-54.

Gray SF, Wyatt JI, Gundersen HJG, et al. Simplified technique for identifying Campylobacter pyloridis. J Clin Pathol 1986; 39:1279-80.

Falsafi T, Mobasheri F, Nariman F, and Najafi M. Susceptibilities to different antibiotics of Helicobacter pylori strains isolated from patients at the pediatric medical center of Tehran, Iran. J Clin Microbiol 2004; 42(1):387-9.

Wikinson SM, Uhi JR, Kline BC and Cockerill FR. Assessment of invasion frequencies of cultured HEp-2 cells by clinical Isolates of Helicobacter pylori using an acridine orange assay. J Clin Pathol. 1998; 51:127-133.

Kim, S. S; H. S. Lee, Y. S. Cho, Y. S. Lee, C. S. Bhang, H. S. Chae, S. W. Han, I. S. Chung, and D. H. Park. The Effect of the Repeated Subcultures of Helicobacter pylori on adhesion, motility, cytotoxicity, and gastric inflammation. J Korean Med Sci 2002; 17:302-6.

Ismail S, Hampton MB, and Keenan JI. Helicobacter pylori outer membrane vesicles modulates proliferation and interleukin-8 production by gastric epithelial cells. Infect Immun 2003; 71(10):5670-5675.

Guruge JL, Falk PG, Lorenz RG, Dans M, Wirth HP, Blaser MJ, Berg DE, and Gordon JI. Epithelial attachment alters the outcome of Helicobacter pylori Infection. P N A S 1998; 95:3925-30.

Peek Jr. RM, Thompson SA, Donahue JP, Tham KT, Atherton JC, Blaser MJ, and Miller GG. Adherence to gastric epithelial cells induces expression of a Helicobacter pylori gene, iceA that is associated with clinical outcome. Proc Assoc Am Physicians 1998; 110(6):531-44.

Linden SK, Wickstrom C, Lindell G, Gilshenan K, Caristedt I. Four modes of adhesion are used during Helicobacter pylori binding to human mucins in the oral and gastric niches. Helicobacter 2008; 13(2):81-93.

Files
IssueVol 1 No 1 (2009) QRcode
SectionArticles
Keywords
Helicobacter pylori Children Gastr itis Adherence HEp-2 KB cell line

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
How to Cite
1.
Falsafi T, Mahboubi M, Zargampour Z, Ahmadi M. Association between efficient adhesion to HEp-2 cells and severity of gastritis in Helicobacter pylori strains isolated from children. Iran J Microbiol. 1;1(1):23-30.