Divergent effects of Nitric oxide on airway epithelial cell activation

Nitric oxide (NO*) is a gaseous mediator synthesized by Nitric oxide sinthases. NO* is involved in the modulation of inflammation, but its role in airway inflammation remains controversial. We investigated the role of NO* in the synthesis of the chemok Nes Interleukin-8 and Monocyte Chemotactic Prot...

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Autores principales: Neri,Tommaso, Conti,Ilaria, Cerri,Chiara, Tavanti,Laura, Paggiaro,Pierluigi, Celi,Alessandro
Lenguaje:English
Publicado: Sociedad de Biología de Chile 2010
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602010000400012
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spelling oai:scielo:S0716-976020100004000122011-02-01Divergent effects of Nitric oxide on airway epithelial cell activationNeri,TommasoConti,IlariaCerri,ChiaraTavanti,LauraPaggiaro,PierluigiCeli,Alessandro Adhesion molecules Airway inflammation Alveolar Epithelium Chemok Nes Nitric Oxide Nitric oxide (NO*) is a gaseous mediator synthesized by Nitric oxide sinthases. NO* is involved in the modulation of inflammation, but its role in airway inflammation remains controversial. We investigated the role of NO* in the synthesis of the chemok Nes Interleukin-8 and Monocyte Chemotactic Protein-1, and of Intercellular Adhesion Molecule-1 by human airway epithelial cells. normal human bronchial epithelial cells and the bronchial epithelial cell line BEAS-2B were used. Neterleukin-8 (IL-8) and Monocyte Chemotactic Protein-1 (MCP-1) secretion and Intercellular Adhesion Molecule-1 (ICAM-1) expression were measured by ELISA. mRNA was assessed by semiquantitative RTI-PCR. Neterleukin-8 secretion was significantly reduced after 24h incubation with the NO* donor, sodium nitroprusside. The effect was dose-dependent. Similar results were obta Ned with S-Nitroso-N-D,L-penicillam Ne and S-Nitroso-L-glutathione. Inhibition of endogenous NO* with the Nitric oxide synthase inhibitor N-Nitro-L-arg N Ne-methyl-esther caused an increase in IL-8 secretion by lypopolisaccharide- and cytok Ne-stimulated BEAS-2B cells. Sodium nitroprusside also caused a reduction in Monocyte Chemotactic Protein-1 secretion by both cell types. In contrast, Intercellular Adhesion Molecule-1 expression was upregulated by sodium NItroprusside. RTI-PCR results indícate that the modulation of protein levels was paralleled by modification in mRNA levels. NO* has divergent effects on the synthesis of different inflammatory mediators in human bronchial epithelial cells.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.43 n.4 20102010-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602010000400012en10.4067/S0716-97602010000400012
institution Scielo Chile
collection Scielo Chile
language English
topic Adhesion molecules
Airway inflammation
Alveolar Epithelium
Chemok Nes
Nitric Oxide
spellingShingle Adhesion molecules
Airway inflammation
Alveolar Epithelium
Chemok Nes
Nitric Oxide
Neri,Tommaso
Conti,Ilaria
Cerri,Chiara
Tavanti,Laura
Paggiaro,Pierluigi
Celi,Alessandro
Divergent effects of Nitric oxide on airway epithelial cell activation
description Nitric oxide (NO*) is a gaseous mediator synthesized by Nitric oxide sinthases. NO* is involved in the modulation of inflammation, but its role in airway inflammation remains controversial. We investigated the role of NO* in the synthesis of the chemok Nes Interleukin-8 and Monocyte Chemotactic Protein-1, and of Intercellular Adhesion Molecule-1 by human airway epithelial cells. normal human bronchial epithelial cells and the bronchial epithelial cell line BEAS-2B were used. Neterleukin-8 (IL-8) and Monocyte Chemotactic Protein-1 (MCP-1) secretion and Intercellular Adhesion Molecule-1 (ICAM-1) expression were measured by ELISA. mRNA was assessed by semiquantitative RTI-PCR. Neterleukin-8 secretion was significantly reduced after 24h incubation with the NO* donor, sodium nitroprusside. The effect was dose-dependent. Similar results were obta Ned with S-Nitroso-N-D,L-penicillam Ne and S-Nitroso-L-glutathione. Inhibition of endogenous NO* with the Nitric oxide synthase inhibitor N-Nitro-L-arg N Ne-methyl-esther caused an increase in IL-8 secretion by lypopolisaccharide- and cytok Ne-stimulated BEAS-2B cells. Sodium nitroprusside also caused a reduction in Monocyte Chemotactic Protein-1 secretion by both cell types. In contrast, Intercellular Adhesion Molecule-1 expression was upregulated by sodium NItroprusside. RTI-PCR results indícate that the modulation of protein levels was paralleled by modification in mRNA levels. NO* has divergent effects on the synthesis of different inflammatory mediators in human bronchial epithelial cells.
author Neri,Tommaso
Conti,Ilaria
Cerri,Chiara
Tavanti,Laura
Paggiaro,Pierluigi
Celi,Alessandro
author_facet Neri,Tommaso
Conti,Ilaria
Cerri,Chiara
Tavanti,Laura
Paggiaro,Pierluigi
Celi,Alessandro
author_sort Neri,Tommaso
title Divergent effects of Nitric oxide on airway epithelial cell activation
title_short Divergent effects of Nitric oxide on airway epithelial cell activation
title_full Divergent effects of Nitric oxide on airway epithelial cell activation
title_fullStr Divergent effects of Nitric oxide on airway epithelial cell activation
title_full_unstemmed Divergent effects of Nitric oxide on airway epithelial cell activation
title_sort divergent effects of nitric oxide on airway epithelial cell activation
publisher Sociedad de Biología de Chile
publishDate 2010
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602010000400012
work_keys_str_mv AT neritommaso divergenteffectsofnitricoxideonairwayepithelialcellactivation
AT contiilaria divergenteffectsofnitricoxideonairwayepithelialcellactivation
AT cerrichiara divergenteffectsofnitricoxideonairwayepithelialcellactivation
AT tavantilaura divergenteffectsofnitricoxideonairwayepithelialcellactivation
AT paggiaropierluigi divergenteffectsofnitricoxideonairwayepithelialcellactivation
AT celialessandro divergenteffectsofnitricoxideonairwayepithelialcellactivation
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