The neutrophil-activating protein of Helicobacter pylori crosses endothelia to promote neutrophil adhesion in vivo

Alessandra Polenghi, Fleur Bossi, Fabio Fischetti, Paolo Durigutto, Anna Cabrelle, Nicola Tamassia, Marco A. Cassatella, Cesare Montecucco, Francesco Tedesco, Marina De Bernard

Research output: Contribution to journalArticlepeer-review

Abstract

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 β2 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.

Original languageEnglish
Pages (from-to)1312-1320
Number of pages9
JournalJournal of Immunology
Volume178
Issue number3
Publication statusPublished - Feb 1 2007

ASJC Scopus subject areas

  • Immunology

Fingerprint

Dive into the research topics of 'The neutrophil-activating protein of Helicobacter pylori crosses endothelia to promote neutrophil adhesion in vivo'. Together they form a unique fingerprint.

Cite this