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Substance P: a neurogenic mediator of acute cellular inflammation in the dog?
Author(s) -
THOMSEN M. KROGSGAARD
Publication year - 1991
Publication title -
journal of veterinary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.527
H-Index - 60
eISSN - 1365-2885
pISSN - 0140-7783
DOI - 10.1111/j.1365-2885.1991.tb00834.x
Subject(s) - mediator , substance p , inflammation , neurogenic inflammation , stimulation , priming (agriculture) , in vivo , receptor , chemistry , pathogenesis , leukotriene b4 , in vitro , pharmacology , neuropeptide , microbiology and biotechnology , immunology , biology , medicine , biochemistry , botany , germination
Substance P (SP) is a neuropeptide that has recently been implicated in the pathogenesis of neurogenic inflammation. SP has been shown to activate polymorphonuclear leukocytes (PMN) as well as other inflammatory cells. The present study investigated the direct stimulatory and priming effects of SP on canine PMN aggregation and migration. Direct stimulation of cell migration by SP was present at an unphysiologically high concentration of the mediator. However, when micromolar concentrations of SP were added to PMN prior to stimulation with sub‐optimal concentrations of leukotriene B 4 (LTB 4 ), the cells exhibited enhanced aggregation and migration, i.e. priming, when stimulated with the latter. Since SP has been reported to act via the formyl‐Met‐Leu‐Phe (fMLP) chemotaxin receptor, this mediator was also studied and found not to possess any effects similar to SP. Thus, the results indicate that SP acts as a primer of canine PMN functions in vitro via a receptor different from that for fMLP. Before ascribing SP a mediator role in canine neurogenic inflammation, in vivo studies determining the concentrations of, and responses to SP in inflamed tissue should be performed.