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Science 26 July 2002: Vol. 297. no. 5581, pp. 573 - 578 DOI: 10.1126/science.1069076
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Research Articles
Helicobacter pylori SabA Adhesin in Persistent Infection and Chronic Inflammation
Jafar Mahdavi,1*
Berit Sondén,1*
Marina Hurtig,1*
Farzad O. Olfat,12
Lina Forsberg,1
Niamh Roche,3
Jonas Ångström,3
Thomas Larsson,3
Susann Teneberg,3
Karl-Anders Karlsson,3
Siiri Altraja,4
Torkel Wadström,5
Dangeruta Kersulyte,6
Douglas E. Berg,6
Andre Dubois,7
Christoffer Petersson,8
Karl-Eric Magnusson,8
Thomas Norberg,9
Frank Lindh,10
Bertil B. Lundskog,11
Anna Arnqvist,112
Lennart Hammarström,13
Thomas Borén1
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.
1 Department of Odontology/Oral Microbiology,
Umeå University, SE-901 87 Umeå, Sweden.
2 The
Swedish Institute for Infectious Disease Control, SE-171 82 Solna,
Sweden.
3 Institute of Medical Biochemistry,
Göteborg University, Box 440, SE-405 30 Göteborg, Sweden.
4 Institute of Molecular and Cell Biology, Tartu
University, EE-51010 Tartu, Estonia.
5 Department of
Infectious Diseases and Medical Microbiology, Lund University, SE-223
62 Lund, Sweden.
6 Department of Molecular
Microbiology, Washington University Medical School, St. Louis, MO
63110, USA.
7 Laboratory of Gastrointestinal and
Liver Studies, Department of Medicine, USUHS, Bethesda, MD 20814-4799,
USA.
8 Department of Molecular and Clinical
Medicine, Division of Medical Microbiology, Linköping University,
SE-581 85 Linköping, Sweden.
9 Department of
Chemistry, Swedish University of Agricultural Sciences, SE-750 07 Uppsala, Sweden.
10 IsoSep AB, Dalkärrsv. 11, SE-146 36 Tullinge, Sweden.
11 Department of
Medical Biosciences/Clinical Cytology, Umeå University, SE-901 87 Umeå, Sweden.
12 Department of Molecular Biology,
Umeå University, SE-901 87 Umeå, Sweden.
13 Center for Biotechnology, Karolinska Institute,
Novum, SE-141 57 Huddinge, Sweden.
*
These authors contributed equally to this work.
Present address: Unité de Génétique
Mycobactérienne, Institut Pasteur, 25 rue du Dr Roux, 75724 Paris
Cedex 15, France.
To whom correspondence should be addressed. E-mail:
Thomas.Boren{at}odont.umu.se
Read the Full Text
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185, 2927-2935
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- The impact of parietal cells on Helicobacter pylori tropism and host pathology: An analysis using gnotobiotic normal and transgenic mice.
- A. J. Syder, J. D. Oh, J. L. Guruge, D. O'Donnell, M. Karlsson, J. C. Mills, B. M. Bjorkholm, and J. I. Gordon (2003)
PNAS
100, 3467-3472
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- Emergence of Tetracycline Resistance in Helicobacter pylori: Multiple Mutational Changes in 16S Ribosomal DNA and Other Genetic Loci.
- D. Dailidiene, M. T. Bertoli, J. Miciuleviciene, A. K. Mukhopadhyay, G. Dailide, M. A. Pascasio, L. Kupcinskas, and D. E. Berg (2002)
Antimicrob. Agents Chemother.
46, 3940-3946
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