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Mediators of Inflammation
Volume 4, Issue 4, Pages 273-281
http://dx.doi.org/10.1155/S0962935195000445

Effect of dexamethasone on carrageenin-induced inflammation in the lung

1Department of Medicine, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6 8RF, UK
2Department of Histopathology, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6 8RF, UK
3Electron Microscopy Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK
4Department of Histopathology, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK

Copyright © 1995 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

To study the anti-inflammatory mechanisms of glucocorticoids, we have compared the effects of intratracheal carrageenin (2.5 mg) on control rats and those in which inflammation was subdued by prior dexamethasone treatment (10 mg/l in drinking water). Inflammation was maximal 48 h post-carrageenin. After dexamethasone, carrageenin caused tittle inflammation or oedema (wet lung (mg), n = 6, mean ± S.E.M.; control, 995 ± 51; carrageenin + dexamethasone, 1144 ± 83; compared with carrageenin alone, 1881 ± 198), but rats had more lung lavage neutrophils than those given carrageenin alone (PMN × 106 /lung, mean ± S.E.M.; control, 0.055 ± 0.003; carrageenin + dexamethasone, 8.54 ± 1.52; compared with carrageenin alone, 6.30 ± 1.71). Proteolysis and partial inactivation of the anti-inflammatory mediator, lipocortin 1 (Lcl), in carrageenin-instilled rats was offset in those also given dexamethasone, by increased Lc1 levels (intact Lc1 ng/ml lavage fluid, n = 4, mean ± S.E.M.; control 24 ± 6; carrageenin 15 ± 4; carrageenin + dexamethasone, 40 ± 15). Maintenance of sufficient intact (fully active) extracellular Lc1 may contribute to the actions of glucocorticoids.