HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 280, Issue 15, 15390-15397, April 15, 2005

This Article Full Text Full Text (PDF) All Versions of this Article: 280/15/15390    most recent M412725200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Unemo, M. Articles by Teneberg, S. Search for Related Content PubMed PubMed Citation Articles by Unemo, M. Articles by Teneberg, S. Social Bookmarking                      What's this?

The Sialic Acid Binding SabA Adhesin of Helicobacter pylori Is Essential for Nonopsonic Activation of Human Neutrophils^*

Magnus Unemo, Marina Aspholm-Hurtig¶, Dag Ilver||, Jörgen Bergström||, Thomas Borén, Dan Danielsson, and Susann Teneberg||**

From the Department of Clinical Microbiology, Örebro University Hospital, SE 701 85 Örebro, the Department of Medical Biochemistry and Biophysics, Umeå University, SE 901 87 Umeå, and the ^||Institute of Medical Biochemistry, Göteborg University, P. O. Box 440, SE 405 30 Göteborg, Sweden

Infiltration of neutrophils and monocytes into the gastric mucosa is a hallmark of chronic gastritis caused by Helicobacter pylori. Certain H. pylori strains nonopsonized stimulate neutrophils to production of reactive oxygen species causing oxidative damage of the gastric epithelium. Here, the contribution of some H. pylori virulence factors, the blood group antigen-binding adhesin BabA, the sialic acid-binding adhesin SabA, the neutrophil-activating protein HP-NAP, and the vacuolating cytotoxin VacA, to the activation of human neutrophils in terms of adherence, phagocytosis, and oxidative burst was investigated. Neutrophils were challenged with wild type bacteria and isogenic mutants lacking BabA, SabA, HP-NAP, or VacA. Mutant and wild type strains lacking SabA had no neutrophil-activating capacity, demonstrating that binding of H. pylori to sialylated neutrophil receptors plays a pivotal initial role in the adherence and phagocytosis of the bacteria and the induction of the oxidative burst. The link between receptor binding and oxidative burst involves a G-protein-linked signaling pathway and downstream activation of phosphatidylinositol 3-kinase as shown by experiments using signal transduction inhibitors. Collectively our data suggest that the sialic acid-binding SabA adhesin is a prerequisite for the nonopsonic activation of human neutrophils and, thus, is a virulence factor important for the pathogenesis of H. pylori infection.

Received for publication, November 10, 2004 , and in revised form, January 24, 2005.

^* This study was supported in part by the Swedish Medical Research Council (Grants 12628/ST and 11218/TB), the Swedish Cancer Foundation (Projects 4128-B03-06XCC/ST and 4101-B00-03XAB/TB), the Swedish Medical Society/The Foundations of the National Board of Health and Welfare (to S. T.), Volvo Assar Gabrielssons Foundation (to S. T.), Umeå University Bio-Technology Foundation, County Council of Västerbotten, and Stiftelserna JC Kempe och Seth M Kempes Minne (to T. B.), the Research Committee of Örebro County (to D. D.), and the Örebro University Hospital Research Foundation (to D. D.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ Supported by a grant from the Foundation for Strategic Research/Program "Infection & Vaccinology."

^** To whom correspondence should be addressed. Tel.: 46-31-773-3492; Fax: 46-31-413-190; E-mail: Susann.Teneberg{at}medkem.gu.se.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				H. M. S. Algood and T. L. Cover Helicobacter pylori Persistence: an Overview of Interactions between H. pylori and Host Immune Defenses Clin. Microbiol. Rev., October 1, 2006; 19(4): 597 - 613. [Abstract] [Full Text] [PDF]

				J. G. Kusters, A. H. M. van Vliet, and E. J. Kuipers Pathogenesis of Helicobacter pylori Infection Clin. Microbiol. Rev., July 1, 2006; 19(3): 449 - 490. [Abstract] [Full Text] [PDF]

				R. M. Peek Jr. Events at the Host-Microbial Interface of the Gastrointestinal Tract IV. The pathogenesis of Helicobacter pylori persistence Am J Physiol Gastrointest Liver Physiol, July 1, 2005; 289(1): G8 - G12. [Abstract] [Full Text] [PDF]

				H. Miller-Podraza, B. Lanne, J. Angstrom, S. Teneberg, M. A. Milh, P.-A. Jovall, H. Karlsson, and K.-A. Karlsson Novel Binding Epitope for Helicobacter pylori Found in Neolacto Carbohydrate Chains: STRUCTURE AND CROSS-BINDING PROPERTIES J. Biol. Chem., May 20, 2005; 280(20): 19695 - 19703. [Abstract] [Full Text] [PDF]