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Leukotriene B 4 and prostaglandin E 2 mediate the inflammatory response of rabbit skin to intradermal arachidonic acid
Author(s) -
Aked D.M.,
Foster S.J.
Publication year - 1987
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1987.tb11355.x
Subject(s) - arachidonic acid , leukotriene b4 , eicosanoid , extravasation , prostaglandin e2 , leukotriene , chemistry , inflammation , prostaglandin , lipoxygenase , prostaglandin e , pharmacology , infiltration (hvac) , anti inflammatory , endocrinology , medicine , immunology , biochemistry , enzyme , physics , asthma , thermodynamics
1 Acute inflammation was induced in rabbit skin by intradermal injection of arachidonic acid. 2 Inflammation was assessed by the local accumulation of intravenously‐injected 125 I‐serum albumin (plasma extravasation) and histologically (polymorphonuclear leucocyte, PMNL infiltration). 3 Leukotriene B 4 (LTB 4 ) and prostaglandin E 2 (PGE 2 ) were extracted from skin and fractionated using C 18 mini‐columns. They were quantitated by specific radioimmunoassays and authenticated by reversed‐phase high performance liquid chromatography analysis. 4 Maximally elevated levels of LTB 4 and PGE 2 were detected in skin 5 min after arachidonic acid injection. At subsequent times the eicosanoid content of the skin decreased. 5 The decrease in the eicosanoid content of the skin was due to rapid clearance ( t 1/2 approximately 5 min) via the microvasculature and not a consequence of metabolism. 6 The concentration of LTB 4 and PGE 2 measured in inflamed skin was sufficient to account for the plasma extravasation and PMNL infiltration induced by arachidonic acid. The model therefore is useful for evaluating the anti‐inflammatory efficacy of inhibitors of arachidonic acid metabolism including 5‐lipoxygenase inhibitors. 7 The consequences of the rapid clearance of LTB 4 from inflammatory sites are discussed with respect to its measurement in inflammatory disease and its role as an acute inflammatory mediator.