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

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Abstract
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.

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