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Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.

Nitric oxide (NO), produced by alveolar macrophages (AM) is used as a marker of respiratory tract inflammation. Lipocortin 1 (Lc-1) is an anti-inflammatory, glucocorticoid-inducible protein. The current aims were to determine whether (a) an Lc-1-derived peptide, Ac2-26, inhibited lipopolysaccharide...

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Detalles Bibliográficos
Autores principales: Kamal, A M, Tetley, T D, Witherden, I R, Smith, S F
Formato: Texto
Lenguaje:English
Publicado: 1998
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1781829/
https://www.ncbi.nlm.nih.gov/pubmed/9836495
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author Kamal, A M
Tetley, T D
Witherden, I R
Smith, S F
author_facet Kamal, A M
Tetley, T D
Witherden, I R
Smith, S F
author_sort Kamal, A M
collection PubMed
description Nitric oxide (NO), produced by alveolar macrophages (AM) is used as a marker of respiratory tract inflammation. Lipocortin 1 (Lc-1) is an anti-inflammatory, glucocorticoid-inducible protein. The current aims were to determine whether (a) an Lc-1-derived peptide, Ac2-26, inhibited lipopolysaccharide (LPS)-induced NO release by primary AM in vitro and (b) the inhibitory action of dexamethasone was Lc-1-dependent. LPS treatment stimulated NO release from rat AM. Ac2-26 had little effect on unstimulated release, but suppressed LPS-stimulated release at concentrations > or =320 nM (320 nM, 10 +/- 3%; 3.2 microM, 15 +/- 3%; 32 microM, 27 +/- 4% NO inhibited, mean +/- SEM, n = 6). Inhibition by dexamethasone of NO release was unaffected by neutralizing anti-Lc-1 indicating that this action is Lc-1-independent in primary AM. Nevertheless inhibition of NO release by Ac2-26 (80 microM) was similar to that of 1 microM dexamethasone (Ac2-26, 40 +/- 6%; dexamethasone, 48 +/- 6% NO inhibited, mean +/- SEM, n = 6).
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spelling pubmed-17818292007-01-25 Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide. Kamal, A M Tetley, T D Witherden, I R Smith, S F Mediators Inflamm Research Article Nitric oxide (NO), produced by alveolar macrophages (AM) is used as a marker of respiratory tract inflammation. Lipocortin 1 (Lc-1) is an anti-inflammatory, glucocorticoid-inducible protein. The current aims were to determine whether (a) an Lc-1-derived peptide, Ac2-26, inhibited lipopolysaccharide (LPS)-induced NO release by primary AM in vitro and (b) the inhibitory action of dexamethasone was Lc-1-dependent. LPS treatment stimulated NO release from rat AM. Ac2-26 had little effect on unstimulated release, but suppressed LPS-stimulated release at concentrations > or =320 nM (320 nM, 10 +/- 3%; 3.2 microM, 15 +/- 3%; 32 microM, 27 +/- 4% NO inhibited, mean +/- SEM, n = 6). Inhibition by dexamethasone of NO release was unaffected by neutralizing anti-Lc-1 indicating that this action is Lc-1-independent in primary AM. Nevertheless inhibition of NO release by Ac2-26 (80 microM) was similar to that of 1 microM dexamethasone (Ac2-26, 40 +/- 6%; dexamethasone, 48 +/- 6% NO inhibited, mean +/- SEM, n = 6). 1998 /pmc/articles/PMC1781829/ /pubmed/9836495 Text en
spellingShingle Research Article
Kamal, A M
Tetley, T D
Witherden, I R
Smith, S F
Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
title Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
title_full Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
title_fullStr Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
title_full_unstemmed Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
title_short Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
title_sort reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1781829/
https://www.ncbi.nlm.nih.gov/pubmed/9836495
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