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pubmed-article:12672049pubmed:abstractTextInfection 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.lld:pubmed
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pubmed-article:12672049pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:12672049pubmed:articleTitleThe neutrophil-activating protein of Helicobacter pylori (HP-NAP) activates the MAPK pathway in human neutrophils.lld:pubmed
pubmed-article:12672049pubmed:affiliationIstituto Veneto di Medicina Molecolare, Immunologia Clinica, Università di Padova, Padova, Italy. hiroaki.nishioka@pathology.oxford.ac.uklld:pubmed
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pubmed-article:12672049pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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