Cargando…
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...
Autores principales: | , , , |
---|---|
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 |
_version_ | 1782131984108093440 |
---|---|
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). |
format | Text |
id | pubmed-1781829 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1998 |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT kamalam reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide AT tetleytd reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide AT witherdenir reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide AT smithsf reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide |