The neutrophil‐activating protein of Helicobacter pylori (HP‐NAP) activates the MAPK pathway in human neutrophils

Infection by Helicobacter pylori causes an acute inflammatory response followed by a chronic infection of the human gastric mucosa characterized by the infiltration of neutrophils andmononuclear inflammatory cells. The neutrophil‐activating protein of Helicobacter pylori (HP‐NAP) is a virulence fact...

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Bibliographic Details
Published in:European journal of immunology 2003-04, Vol.33 (4), p.840-849
Main Authors: Nishioka, Hiroaki, Baesso, Ilenia, Semenzato, Gianpietro, Trentin, Livio, Rappuoli, Rino, Giudice, Giuseppe Del, Montecucco, Cesare
Format: Article
Language:English
Subjects:
Actins - metabolism
Bacterial Proteins - metabolism
Bacterial Proteins - pharmacology
Cell Adhesion - drug effects
Chemotaxis, Leukocyte - drug effects
Dose-Response Relationship, Drug
Enzyme Inhibitors - pharmacology
Flavonoids - pharmacology
Helicobacter pylori
Humans
Imidazoles - pharmacology
MAP Kinase Signaling System - drug effects
Mitogen-Activated Protein Kinases - antagonists & inhibitors
Mitogen-Activated Protein Kinases - metabolism
Mitogen‐activated protein kinase
Neutrophil
Neutrophil activating protein
Neutrophils - drug effects
Neutrophils - enzymology
Neutrophils - immunology
Pertussis toxin
Pertussis Toxin - pharmacology
Pyridines - pharmacology
Superoxides - metabolism
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Summary:Infection by Helicobacter pylori causes an acute inflammatory response followed by a chronic infection of the human gastric mucosa characterized by the infiltration of neutrophils andmononuclear inflammatory cells. The neutrophil‐activating protein of Helicobacter pylori (HP‐NAP) is a virulence factor that activates neutrophils, monocytes, and mast cells. However, the mechanism by which HP‐NAP activates these cells is not fully understood. Here, we show that HP‐NAP induces extracellular regulated kinase (ERK) and p38‐mitogen‐activated protein kinase (MAPK) activation in human neutrophils; c‐Jun N‐terminal kinase is not activated by HP‐NAP. A MAPK/ERK kinase inhibitor and a p38‐MAPK inhibitor suppress HP‐NAP‐mediated neutrophil oxidative burst, adhesion, andchemotaxis, but not actin polymerization. Pertussis toxin (PTX) inhibits all these neutrophil functions and the MAPK activation caused by HP‐NAP. These results demonstrate that HP‐NAP activates neutrophils through a PTX‐sensitive pathway and that ERK and p38‐MAPK are involved in many neutrophil functions stimulated by HP‐NAP.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.200323726