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Infection and Immunity, June 2002, p. 2908-2914, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.2908-2914.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Lipopolysaccharide-Induced Granule Mobilization and Priming of the Neutrophil Response to Helicobacter pylori Peptide Hp(2-20), Which Activates Formyl Peptide Receptor-Like 1

Johan Bylund,1 Anna Karlsson,1 Francois Boulay,2 and Claes Dahlgren1*

Phagocyte Research Laboratory, Department of Rheumatology, University of Göteborg, Göteborg, Sweden,1 DMBS/BBSI (UMR 5092 CEA/CNRS/UJF), CEA-Grenoble, 38054 Grenoble Cedex 9, France2

Received 9 July 2001/ Returned for modification 11 September 2001/ Accepted 28 February 2002

The cecropin-like bactericidal peptide Hp(2-20) from Helicobacter pylori induces activation of the NADPH oxidase in human neutrophils via formyl peptide receptor-like 1 (FPRL1) (J. Bylund, T. Christophe, F. Boulay, T. Nyström, A. Karlsson, and C. Dahlgren, Antimicrob. Agents Chemother. 45:1700-1704, 2001). Here we investigated the ability of bacterial lipopolysaccharide (LPS) to prime this response. Neutrophils treated with LPS for 30 min at 37°C produced substantially more superoxide anion than control cells upon stimulation with Hp(2-20). Hence, LPS primed the cells for subsequent stimulation through FPRL1. To study the molecular background of this priming phenomenon, we measured the degrees of granule mobilization and concomitant receptor upregulation to the cell surface in LPS-treated cells. Exposure of complement receptors 1 and 3 as well as the formyl peptide receptor (FPR) was markedly increased after LPS treatment. Since approximately 60% of the gelatinase granules were mobilized while the specific granules were retained, we hypothesized that the gelatinase granules were potential stores of FPRL1. The presence of FPRL1 mainly in the gelatinase granules was confirmed by Western blotting of subcellular fractions of resting neutrophils. These results suggest that the mechanism behind the LPS-induced priming of FPRL1-mediated responses lies at the level of granule (receptor) mobilization.

* Corresponding author. Mailing address: Phagocyte Research Laboratory, Department of Rheumatology, Guldhedsgatan 10, S-41346 Göteborg, Sweden. Phone: 46-31-342 46 83. Fax: 46-31-82 88 98. E-mail: claes.dahlgren{at}microbio.gu.se.

Editor: R. N. Moore

Infection and Immunity, June 2002, p. 2908-2914, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.2908-2914.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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