Induction of plasma exudation and inflammatory cell infiltration by leukotriene C4 and leukotriene B4 in mouse peritonitis

Leukotriene induction of the fluid and cellular phases of the inflammatory response in the mouse was evaluated. Intraperitoneal injection of leukotriene C4 (LTC4 250 ng) led to dye extravasation but not polymorphonuclear leukocyte (PMN) infiltration, whereas injection of leukotriene B4 (LTB4 250 ng)...

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Bibliographic Details
Published inInflammation Vol. 15; no. 4; p. 251
Main Authors Griswold, D E, Webb, E F, Hillegass, L M
Format Journal Article
LanguageEnglish
Published United States 01.08.1991
Subjects
Animals
Ascites - chemically induced
Capillary Permeability - drug effects
Chemotaxis, Leukocyte - drug effects
Colchicine - pharmacology
Drug Interactions
Imidazoles - pharmacology
Inflammation
Injections, Intraperitoneal
Leukotriene B4 - administration & dosage
Leukotriene B4 - pharmacology
Leukotriene B4 - toxicity
Male
Mice
Mice, Inbred BALB C
Neutrophils - drug effects
Peritonitis - chemically induced
Peritonitis - pathology
Pyrazoles - pharmacology
SRS-A - administration & dosage
SRS-A - pharmacology
SRS-A - toxicity
Thiazoles - pharmacology
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Summary:Leukotriene induction of the fluid and cellular phases of the inflammatory response in the mouse was evaluated. Intraperitoneal injection of leukotriene C4 (LTC4 250 ng) led to dye extravasation but not polymorphonuclear leukocyte (PMN) infiltration, whereas injection of leukotriene B4 (LTB4 250 ng), led to PMN infiltration but not dye extravasation. The injection of both leukotrienes did not result in synergy. LTC4 did not appear to induce significant release or formation of chemotactic mediators, but the dye extravasation induced by LTC4 was inhibited by the vasoactive amine antagonist cyproheptadine and not by the eicosanoid inhibitors phenidone or naproxen. The response was markedly inhibited by the cytokine and eicosanoid inhibitors SK&F 86002 and SK&F 104493. PMN infiltration induced by LTB4 was not inhibited by SK&F 86002 or phenidone but was abrogated by colchicine treatment. LTB4 in this model did not appear to cause release or formation of vasoactive mediators. These leukotrienes appeared to be independent, complementary, and sufficient to mount a complete inflammatory response in the mouse.
ISSN:0360-3997
DOI:10.1007/BF00917310