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* Department of Biology, University of Padua, Padua, Italy;
Venetian Institute of Molecular Medicine, Padua, Italy;
Department of Physiology and Pathology, University of Trieste, Trieste, Italy;
Department of Medicine and Neurology, University of Trieste, Cattinara Hospital, Trieste, Italy;
¶ Department of Pathology, Division of General Pathology, University of Verona, Verona, Italy; and
|| Department of Biomedical Sciences, University of Padua, Padua, Italy
Helicobacter pylori induces an acute inflammatory response followed by a chronic infection of the human gastric mucosa characterized by infiltration of neutrophils/polymorphonuclear cells (PMNs) and mononuclear cells. The H. pylori neutrophil-activating protein (HP-NAP) activates PMNs, monocytes, and mast cells, and promotes PMN adherence to the endothelium in vitro. By using intravital microscopy analysis of rat mesenteric venules exposed to HP-NAP, we demonstrated, for the first time in vivo, that HP-NAP efficiently crosses the endothelium and promotes a rapid PMN adhesion. This HP-NAP-induced adhesion depends on the acquisition of a high affinity state of 
2 integrin on the plasma membrane of PMNs, and this conformational change requires a functional p38 MAPK. We also show that HP-NAP stimulates human PMNs to synthesize and release a number of chemokines, including CXCL8, CCL3, and CCL4. Collectively, these data strongly support a central role for HP-NAP in the inflammation process in vivo: indeed, HP-NAP not only recruits leukocytes from the vascular lumen, but also stimulates them to produce messengers that may contribute to the maintenance of the flogosis associated with the H. pylori infection.
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1 This work was supported by Italian Association for Cancer Research Regional Grant Proposal 2005 Veneto and Ministero dell’Istruzione, dell’Università e della Ricerca (Grant 2004064334_006; to M.d.B.); Ministero dell’Istruzione, dell’Università e della Ricerca Grant 2005060371_001 and Fondi sulla Ricerca di Base (to M.A.C.); Ministero dell’Istruzione, dell’Università e della Ricerca Grant 2005060371_005 (to F.T.); and Ministero dell’Istruzione, dell’Università e della Ricerca Grant 2005060371_004 (to C.M.).
2 A.P. and F.B. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Marina de Bernard, Venetian Institute of Molecular Medicine, Via Orus 2, 35121 Padua, Italy. E-mail address: marina.debernard{at}unipd.it
4 Abbreviations used in this paper: PMN, polymorphonuclear cell; AO, acridine orange; HP-NAP, H. pylori neutrophil-activating protein; PAF, platelet-activating factor; PET, polycarbonate; RPA, RNase protection assay; RT, room temperature; VEGF, vascular endothelial growth factor.
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