LCB-2183 INHIBITS THE INFLAMMATION ASSOCIATED WITH OXAZOLONE-INDUCED CONTACT SENSITIVITY

Citation
N. Murray et al., LCB-2183 INHIBITS THE INFLAMMATION ASSOCIATED WITH OXAZOLONE-INDUCED CONTACT SENSITIVITY, International journal of immunopharmacology, 16(8), 1994, pp. 675-683
Citations number
36
Categorie Soggetti
Immunology,"Pharmacology & Pharmacy
ISSN journal
01920561
Volume
16
Issue
8
Year of publication
1994
Pages
675 - 683
Database
ISI
SICI code
0192-0561(1994)16:8<675:LITIAW>2.0.ZU;2-V
Abstract
LCB 2183, an anti-allergic and potential anti-asthma compound, has bee n investigated for its ability to inhibit contact sensitivity in the m ouse. The delayed response to epicutaneous hapten challenge in this mo del is a classical T-cell-mediated inflammatory reaction which is depe ndent on an early initiation phase. Both the early and late components of oxazolone-induced contact sensitivity were inhibited by oral admin istration of LCB 2183 in a dose-dependent manner. The drug appears to act on the efferent limb of the response since administration before h apten challenge was effective, while administration before the initial sensitization was not. LCB 2183 acts early in the cascade of events l eading to inflammation, since the initiation phase of the response was inhibited; nonetheless, an effect of the drug on the late acting infl ammatory cells cannot be ruled out. In comparison with oral prednisolo ne, which was also able to inhibit both the early and late components of the response, LCB 2183 was less active. Sodium cromoglycate and ned ocromil sodium, which are poorly absorbed from the gastrointestinal tr act, were tested by intraperitoneal administration. Neither of these a gents significantly altered the delayed response and only nedocromil s odium had a limited inhibitory effect on the early initiation phase. T hus, in this model, LCB 2183 demonstrated more anti-inflammatory poten tial and resembled prednisolone more closely than either nedocromil so dium or sodium cromoglycate. The possible relevance of these effects i n relation, to the inflammation which characterizes human asthma is co nsidered.