<i>Helicobacter pylori</i> SabA Adhesin in Persistent Infection and Chronic Inflammation

Jafar Mahdavi(Umeå University), Berit Sondén(Umeå University), Marina Hurtig(Umeå University), Farzad O. Olfat(Swedish Institute), Lina Forsberg(Umeå University), Niamh Roche(University of Gothenburg), Jonas Ångström(University of Gothenburg), Thomas Larsson(University of Gothenburg), Susann Teneberg(University of Gothenburg), Karl‐Anders Karlsson(University of Gothenburg), Siiri Altraja(University of Tartu), Torkel Wadström(Lund University), Dangeruta Kersulyte(Washington University in St. Louis), Douglas E. Berg(Washington University in St. Louis), A. Dubois(National Institutes of Health), Christoffer Petersson(Linköping University), Karl‐Eric Magnusson(Linköping University), Thomas Norberg(Swedish University of Agricultural Sciences), Frank Lindh(TechnoServe), Bertil Lundskog(Umeå University), Anna Arnqvist(Umeå University), Lennart Hammarström(Karolinska Institutet), Thomas Borén(Umeå University)
Science
July 26, 2002
10.1126/science.1069076
Cited by 919Open Access
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Abstract

Helicobacter pylori adherence in the human gastric mucosa involves specific bacterial adhesins and cognate host receptors. Here, we identify sialyl-dimeric-Lewis x glycosphingolipid as a receptor for H. pylori and show that H. pylori infection induced formation of sialyl-Lewis x antigens in gastric epithelium in humans and in a Rhesus monkey. The corresponding sialic acid-binding adhesin (SabA) was isolated with the "retagging" method, and the underlying sabA gene (JHP662/HP0725) was identified. The ability of many H. pylori strains to adhere to sialylated glycoconjugates expressed during chronic inflammation might thus contribute to virulence and the extraordinary chronicity of H. pylori infection.

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