Abstract
Infection by Helicobacter pylori causes an acute inflammatory response followed by a chronic infection of the human gastric mucosa. A neutrophil-activating protein (HP-NAP) has been identified in H.pylori, and its role in infection and immune response is currently under investigation. Here, we show that HP-NAP induces beta-hexosaminidase release and interleukin-6 production in peritoneal mast cells, two actions which are completely inhibited by pertussis toxin. We also show that in polarized epithelial cell monolayers HP-NAP translocates from the apical to the basolateral domain, where mast cells are located. These findings characterize HP-NAP as an inflammatory factor of H.pylori that is effective from the beginning of the inflammatory cascade.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenocarcinoma / pathology
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Animals
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Bacterial Proteins / pharmacology
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Bacterial Proteins / physiology*
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Calcimycin / pharmacology
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Calcium / physiology
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Cell Polarity
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Chemotactic Factors / pharmacology
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Chemotactic Factors / physiology*
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Colonic Neoplasms / pathology
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Cytoplasmic Granules / metabolism
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Epithelial Cells / drug effects
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Epithelial Cells / metabolism
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Exocytosis / drug effects
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Helicobacter pylori / physiology*
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Histamine Release / drug effects
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Inflammation
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Interleukin-8 / biosynthesis
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Ionophores / pharmacology
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Male
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Mast Cells / drug effects*
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Mast Cells / enzymology
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Mast Cells / physiology
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Peritoneal Cavity / cytology
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Pertussis Toxin
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Protein Transport
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Rats
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Rats, Wistar
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Tumor Cells, Cultured
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Virulence Factors, Bordetella / pharmacology
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beta-N-Acetylhexosaminidases / metabolism
Substances
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Bacterial Proteins
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Chemotactic Factors
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Interleukin-8
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Ionophores
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Virulence Factors, Bordetella
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neutrophil-activating protein A, Helicobacter pylori
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Calcimycin
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Pertussis Toxin
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beta-N-Acetylhexosaminidases
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Calcium