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Infection and Immunity, September 2004, p. 5464-5469, Vol. 72, No. 9
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.9.5464-5469.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
The Children's Research Centre, Our Lady's Hospital for Sick Children, Crumlin,1 The Conway Institute of Biomolecular and Biomedical Research, The Department of Paediatrics, University College Dublin, and The Dublin Molecular Medicine Centre, Belfield, Dublin, Ireland2
Received 7 February 2004/ Returned for modification 12 March 2004/ Accepted 24 April 2004
The effect of Helicobacter pylori infection on human and murine primary gastric cells was determined. CagA was phosphorylated following adherence of H. pylori to primary human gastric cells. However, it did not adhere to human primary duodenal cells or murine gastric cells, and CagA could not be detected in cell lysates. Identification of an easily available animal model of infection in which the organism adheres to gastric mucosal cells would enhance studies of the virulence of H. pylori.
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