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Infection and Immunity, February 2005, p. 761-769, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.761-769.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Helicobacter pylori Induces Transendothelial Migration of Activated Memory T Cells

Karin Enarsson,1* Mikael Brisslert,2 Steffen Backert,3 and Marianne Quiding-Järbrink1

Department of Medical Microbiology and Immunology, Göteborg University Vaccine Research Institute,1 Department of Rheumatology and Inflammation Research, Göteborg University, Gothenburg, Sweden,2 Department of Medical Microbiology, Otto von Guericke University, Magdeburg, Germany3

Received 24 June 2004/ Returned for modification 24 August 2004/ Accepted 20 October 2004

Helicobacter pylori infection is associated with pronounced infiltration of granulocytes and lymphocytes into the gastric mucosa, resulting in active chronic gastritis that may develop into duodenal ulcer disease or gastric adenocarcinoma. Infiltrating T cells play a major role in the pathology of these diseases, but the signals involved in recruitment of T cells from blood to H. pylori-infected tissues are not well understood. We therefore examined H. pylori-induced T-cell transendothelial migration (TEM). The Transwell system, employing a monolayer of human umbilical vein endothelial cells, was used as a model to study TEM. H. pylori induced a significant T-cell migration, compared to spontaneous migration. CD4+ and CD8+ T cells migrated to the same extent in response to H. pylori, whereas there was significantly larger transmigration of memory T cells compared to naive T cells. Both H. pylori culture filtrate and urease induced migration, and the presence of the H. pylori cag pathogenicity island increased TEM. T-cell TEM was mediated by LFA-1-ICAM-1 interactions in accordance with an increased ICAM-1 expression on the endothelial cells after contact with H. pylori. Migrating T cells had increased expression of activation marker CD69 and chemokine receptors CXCR3, CCR4, and CCR9. Furthermore, T cells migrating in response to H. pylori secreted Th1 but not Th2 cytokines upon stimulation. In conclusion, our data indicate that live H. pylori and its secreted products contribute to T-cell recruitment to the gastric mucosa and that the responding T cells have an activated memory Th1 phenotype.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, Göteborg University, Box 435, 405 30 Göteborg, Sweden. Phone: 46-31-773-6214. Fax: 46-31-773-6205. E-mail: karin.enarsson{at}microbio.gu.se.

Editor: J. T. Barbieri

Infection and Immunity, February 2005, p. 761-769, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.761-769.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Svensson, H., Hansson, M., Kilhamn, J., Backert, S., Quiding-Jarbrink, M. (2009). Selective Upregulation of Endothelial E-Selectin in Response to Helicobacter pylori-Induced Gastritis. Infect. Immun. 77: 3109-3116 [Abstract] [Full Text]  
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