Research

Disease association with two Helicobacter pylori duplicate outer membrane protein genes, homB and homA

Monica Oleastro^1,2 , Rita Cordeiro¹ , Yoshio Yamaoka³ , Dulciene Queiroz⁴ , Francis Mégraud^2,5 , Lurdes Monteiro¹ and Armelle Ménard^2,5

¹  Departamento de Doenças Infecciosas, Instituto Nacional Saúde Dr Ricardo Jorge, Av. Padre Cruz, 1649-016 Lisboa, Portugal

²  INSERM U853, 33076 Bordeaux, France

³  Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, 2002 Holcombe Blvd., Houston, Texas 77030, USA

⁴  Laboratório de Pesquisa Bacteriologia, Faculdade de Medicina, UFMG, Av. Alfredo Balena, 190 S/4026 30130-100, Belo Horizonte, Brazil

⁵  Université Victor Segalen Bordeaux 2, Laboratoire de Bactériologie, Bat. 2B RDC Zone Nord, 33076 Bordeaux cedex, France

author email corresponding author email

Gut Pathogens 2009, 1:12doi:10.1186/1757-4749-1-12

Published:	22 June 2009

Abstract

Background

homB encodes a Helicobacter pylori outer membrane protein. This gene was previously associated with peptic ulcer disease (PUD) and was shown to induce activation of interleukin-8 secretion in vitro, as well as contributing to bacterial adherence. Its 90%-similar gene, homA, was previously correlated with gastritis. The present study aimed to evaluate the gastric disease association with homB and homA, as well as with the H. pylori virulence factors cagA, babA and vacA, in 415 H. pylori strains isolated from patients from East Asian and Western countries. The correlation among these genotypes was also evaluated.

Results

Both homB and homA genes were heterogeneously distributed worldwide, with a marked difference between East Asian and Western strains. In Western strains (n = 234, 124 PUD and 110 non-ulcer dyspepsia (NUD), homB, cagA and vacA s1 were all significantly associated with PUD (p = 0.025, p = 0.014, p = 0.039, respectively), and homA was closely correlated with NUD (p = 0.072). In East Asian strains (n = 138, 73 PUD and 65 NUD), homB was found more frequently than homA, and none of these genes was associated with the clinical outcome.

Overall, homB was associated with the presence of cagA (p = 0.043) and vacA s1 (p < 0.001), whereas homA was found more frequently in cagA-negative (p = 0.062) and vacA s2 (p < 0.001) strains.

Polymorphisms in homB and homA copy number were observed, with a clear geographical specificity, suggesting an involvement of these genes in host adaptation. A correlation between the homB two-copy genotype and PUD was also observed, emphasizing the role of homB in the virulence of the strain.

Conclusion

The global results suggest that homB and homA contribute to the determination of clinical outcome.