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Infection by Helicobacter pylori expressing the BabA adhesin is influenced by the secretor phenotype

Azevedo, M (author)
Eriksson, Sara (author)
Umeå universitet,Institutionen för medicinsk kemi och biofysik
Mendes, N (author)
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Serpa, J (author)
Figueiredo, C (author)
Resende, LP (author)
Ruvoën-Clouet, N (author)
Haas, R (author)
Borén, Thomas (author)
Umeå universitet,Institutionen för medicinsk kemi och biofysik
Le Pendu, J (author)
David, L (author)
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 (creator_code:org_t)
Wiley, 2008
2008
English.
In: Journal of Pathology. - : Wiley. - 0022-3417 .- 1096-9896. ; 215:3, s. 308-316
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Helicobacter pylori (Hp) infects half the world's population and causes diverse gastric lesions, from gastritis to gastric cancer. Our aim was to evaluate the significance of secretor and Lewis status in infection and in vitro adherence by Hp expressing BabA adhesin. We enrolled 304 Hp-infected individuals from Northern Portugal. Gastric biopsies, blood and saliva were collected. Polymerase chain reaction (PCR) and immunofluorescence were used to detect BabA+ Hp in gastric biopsies. In vitro adherence by a BabA expressing Hp strain to gastric biopsies was performed. Secretor status was identified by Ulex, a lectin that recognizes secretor-dependent glycan structures in saliva and in gastric mucosa, and by Lewis(a/b) antibodies, and indirectly by identification of an inactivating mutation in the FUT2 gene (G428A). BabA status of infecting Hp was associated with CagA and VacAs1 (p < 0.05), intercellular localization of Hp (p < 0.01) and the presence of intestinal metaplasia (p < 0.05) and degenerative alterations (p < 0.005) in the biopsies. BabA was associated (p < 0.05) with Ulex staining of gastric biopsies and, although not significantly, to absence of homozygosity for FUT2 G428A inactivating polymorphism. In vitro Hp adherence was higher in cases wild-type or heterozygous for FUT2 G428A mutation (p < 0.0001), cases staining for Ulex (p < 0.0001) and a(-)b+ and a(-)b(-) secretor phenotypes (p < 0.001). In conclusion, BabA+ Hp infection/adhesion is secretor-dependent and associated with the severity of gastric lesions.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

Keyword

Helicobacter pylori; blood-group antigen binding adhesin (BabA); Lewis antigens; secretor status; gastritis; intestinal metaplasia; stomach; immunofluorescence

Publication and Content Type

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