http://www.cnr.it/ontology/cnr/individuo/prodotto/ID12269
Acetylcholine mediates the release of IL-8 in human bronchial epithelial cells by a NFkB/ERK-dependent mechanism (Articolo in rivista)
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- Label
- Acetylcholine mediates the release of IL-8 in human bronchial epithelial cells by a NFkB/ERK-dependent mechanism (Articolo in rivista) (literal)
- Anno
- 2008-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.ejphar.2007.12.029 (literal)
- Alternative label
Mirella Profita a,* ; Anna Bonanno a; Liboria Siena a; Maria Ferraro a,d; Angela M. Montalbano a,c; Flora Pompeo a; Loredana Riccobono a; Michael P. Pieper b; Mark Gjomarkaj a (2008)
Acetylcholine mediates the release of IL-8 in human bronchial epithelial cells by a NFkB/ERK-dependent mechanism
in European journal of pharmacology
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Mirella Profita a,* ; Anna Bonanno a; Liboria Siena a; Maria Ferraro a,d; Angela M. Montalbano a,c; Flora Pompeo a; Loredana Riccobono a; Michael P. Pieper b; Mark Gjomarkaj a (literal)
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- a Institute of Biomedicine and Molecular Immunology, Italian National Research Council, Palermo, Italy
b Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany
c Dipartimento di Biopatologia e Metodologie Biomediche-Sezione di Patologia Generale, Italy
d Dipartimento di Anestesiologia, Rianimazione e delle Emergenze- Università degli Studi di Palermo-Palermo- ITALY (literal)
- Titolo
- Acetylcholine mediates the release of IL-8 in human bronchial epithelial cells by a NFkB/ERK-dependent mechanism (literal)
- Abstract
- Acetylcholine may play a role in cell activation and airway inflammation. We evaluated the levels of both mRNA and protein of muscarinic M1,
M2, M3 receptors in human bronchial epithelial cell line (16HBE). 16HBE cells were also stimulated with acetylcholine and extracellular signalregulated
kinase1/2 (ERK1/2) and NFkB pathway activation as well as the IL-8 release was assessed in the presence or absence of the inhibitor of
Protein-kinase (PKC) (GF109203X), of the inhibitor of mitogenic activated protein-kinase kinase (MAPKK) (PDO9805), of the inhibitor of kinaseB-
? phosphorilation (pIkB?) (BAY11-7082), and of muscarinic receptor antagonists tiotropium bromide, 4-Diphenylacetoxy-N-methylpiperidine
methiodide (4-DAMP), telenzepine, gallamine. Additionally, we tested the IL-8-mediated neutrophil chemotactic activity of 16HBE supernatants
stimulated with acetylcholine in the presence or absence of tiotropium. 16HBE cells expressed both protein and mRNA for muscarinic M3, M2 and
M1 receptors with levels of muscarinic M3 receptorNmuscarinic M1 receptorNmuscarinic M2 receptor. Acetylcholine (10 ?M) significantly
stimulated ERK1/2 and NFkB activation as well as IL-8 release in 16HBE cells when compared to basal values. Furthermore, while the use of
tiotropium, 4-DAMP, GF109203X, PDO98059, BAY11-7082 completely abolished these events, the use of telenzepine and gallamine were only
partially able to downregulate these effects. Additionally, acetylcholine-mediated IL-8 release from 16HBE cells significantly increased chemotaxis
toward neutrophils and this effect was blocked by tiotropium. In conclusion, acetylcholine activates the release of IL-8 from 16HBE involving PKC,
ERK1/2 and NFkB pathways via muscarinic receptors, suggesting that it is likely to contribute to IL-8 related neutrophilic inflammatory disorders in
the airway. Thus, muscarinic antagonists may contribute to control inflammatory processes in airway diseases. (literal)
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