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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| Format: | Article |
| Language: | English |
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Wiley
1998-01-01
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| Series: | Mediators of Inflammation |
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| Online Access: | http://dx.doi.org/10.1080/09629359891234 |
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| author | A. M. Kamal T. D. Tetley I. R. Witherden S. F. Smith |
| author_facet | A. M. Kamal T. D. Tetley I. R. Witherden S. F. Smith |
| author_sort | A. M. Kamal |
| collection | DOAJ |
| 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 of 320 nM (320 nM, 10 ± 3%; 3.2 μ M, 15 ± 3%; 32 μ M, 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 Lc1-independent in primary AM. Nevertheless inhibition of NO release by Ac2-26 (80 μ M) was similar to that of 1 μ M dexamethasone (Ac2-26, 40 ± 6%; dexamethasone, 48 ± 6% NO inhibited, mean ± SEM, n=6). |
| format | Article |
| id | doaj-art-c8bcd461d50747a1beac7a286319b4e8 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 1998-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-c8bcd461d50747a1beac7a286319b4e82025-02-03T01:03:19ZengWileyMediators of Inflammation0962-93511466-18611998-01-0172939810.1080/09629359891234Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptideA. M. Kamal0T. D. Tetley1I. R. Witherden2S. F. Smith3Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKDepartment of Respiratory Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKDepartment of Respiratory Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKDepartment of Respiratory Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UKNitric 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 of 320 nM (320 nM, 10 ± 3%; 3.2 μ M, 15 ± 3%; 32 μ M, 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 Lc1-independent in primary AM. Nevertheless inhibition of NO release by Ac2-26 (80 μ M) was similar to that of 1 μ M dexamethasone (Ac2-26, 40 ± 6%; dexamethasone, 48 ± 6% NO inhibited, mean ± SEM, n=6).http://dx.doi.org/10.1080/09629359891234Lipocortin peptideglucocorticoidnitric oxidealveolar macrophagedexamethasone. |
| spellingShingle | A. M. Kamal T. D. Tetley I. R. Witherden S. F. Smith Reduction of nitric oxide release from alveolar macrophages by a lipocortin peptide Mediators of Inflammation Lipocortin peptide glucocorticoid nitric oxide alveolar macrophage dexamethasone. |
| 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 | Lipocortin peptide glucocorticoid nitric oxide alveolar macrophage dexamethasone. |
| url | http://dx.doi.org/10.1080/09629359891234 |
| work_keys_str_mv | AT amkamal reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide AT tdtetley reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide AT irwitherden reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide AT sfsmith reductionofnitricoxidereleasefromalveolarmacrophagesbyalipocortinpeptide |