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Infection and Immunity, July 2009, p. 3109-3116, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.01460-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Selective Upregulation of Endothelial E-Selectin in Response to Helicobacter pylori-Induced Gastritis{triangledown}

Helena Svensson,1* Malin Hansson,1 Jan Kilhamn,1 Steffen Backert,2 and Marianne Quiding-Järbrink1

Institute of Biomedicine, Department of Microbiology and Immunology, University of Gothenburg, Box 435, 405 30 Göteborg, Sweden,1 School of Biomolecular and Biomedical Sciences, University College Dublin, Ardmore House, Belfield Campus, Dublin 4, Ireland2

Received 1 December 2008/ Returned for modification 9 February 2009/ Accepted 19 April 2009

Helicobacter pylori is one of the most common bacterial pathogens, infecting up to 50% of the world's population. The host is not able to clear the infection, leading to life-long chronic inflammation with continuous infiltration of lymphocytes and granulocytes. The migration of leukocytes from the blood into inflamed tissue is dependent on adhesion molecules expressed on the vascular endothelium. The aim of this study was to characterize the effect of H. pylori-induced gastritis with regard to the expression of endothelial adhesion molecules in the gastric mucosa and compare this to other types of chronic mucosal inflammations. Our results demonstrate an increased level of expression of the adhesion molecule E-selectin, but not of intracellular adhesion molecule 1, vascular adhesion molecule 1, or vascular adhesion protein 1, in H. pylori-induced gastritis but not in gastritis induced by acetylsalicylic acid or pouchitis. The upregulated E-selectin expression was determined to be localized to the gastric mucosa rather than being a systemic response to the infection. Moreover, the H. pylori type IV secretion system encoded by the cag pathogenicity island (cagPAI) was found to be an important determinant for the upregulation of human endothelial E-selectin expression in vitro, and this process is probably dependent on the CagL protein, mediating binding to {alpha}5β1 integrins. Thus, endothelial E-selectin expression induced by H. pylori probably contributes to the large influx of neutrophils and macrophages seen in infected individuals, and our results suggest that this process may be more pronounced in patients infected with cagPAI-positive H. pylori strains and may thereby contribute to tissue damage in these individuals.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, The Sahlgrenska Academy at the University of Gothenburg, Box 435, 405 30 Göteborg, Sweden. Phone: 46-31-7866221. Fax: 46-31-7866205. E-mail: helena.svensson{at}microbio.gu.se

{triangledown} Published ahead of print on 4 May 2009.

Editor: S. R. Blanke

Infection and Immunity, July 2009, p. 3109-3116, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.01460-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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