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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2003-4-2
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pubmed:abstractText |
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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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Bacterial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Flavonoids,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/PD 98059,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Pyridines,
http://linkedlifedata.com/resource/pubmed/chemical/SB 203580,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides,
http://linkedlifedata.com/resource/pubmed/chemical/neutrophil-activating protein A...
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
33
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
840-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12672049-Actins,
pubmed-meshheading:12672049-Bacterial Proteins,
pubmed-meshheading:12672049-Cell Adhesion,
pubmed-meshheading:12672049-Chemotaxis, Leukocyte,
pubmed-meshheading:12672049-Dose-Response Relationship, Drug,
pubmed-meshheading:12672049-Enzyme Inhibitors,
pubmed-meshheading:12672049-Flavonoids,
pubmed-meshheading:12672049-Humans,
pubmed-meshheading:12672049-Imidazoles,
pubmed-meshheading:12672049-MAP Kinase Signaling System,
pubmed-meshheading:12672049-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12672049-Neutrophils,
pubmed-meshheading:12672049-Pertussis Toxin,
pubmed-meshheading:12672049-Pyridines,
pubmed-meshheading:12672049-Superoxides
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pubmed:year |
2003
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pubmed:articleTitle |
The neutrophil-activating protein of Helicobacter pylori (HP-NAP) activates the MAPK pathway in human neutrophils.
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pubmed:affiliation |
Istituto Veneto di Medicina Molecolare, Immunologia Clinica, Università di Padova, Padova, Italy. hiroaki.nishioka@pathology.oxford.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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