作者: JD Levine , J Gooding , P Donatoni , L Borden , EJ Goetzl
DOI: 10.1523/JNEUROSCI.05-11-03025.1985
关键词:
摘要: The results of recent studies the mechanism leukotriene B4-induced hyperalgesia suggest a dependence on polymorphonuclear leukocytes (PMNLs). In this study, we addressed contribution PMNLs to evoked by peptide chemotactic factors N-formyl-methionyl-leucyl-phenylalanine (fMLP) and anaphylatoxin fragment fifth component complement pathway (C5a). Local injection glycogen, which attracts but does not activate PMNLs, produced marked shift left (toward lower concentrations) in concentration curve fMLP-induced hyperalgesia. addition, PMNL repletion transfusion with syngeneic reestablished PMNL-depleted rats. Finally, supernatants from rat human that had been stimulated fMLP vitro, Preliminary characterization hyperalgesia-inducing activity released indicated it is lipid nature. nonsteroidal anti-inflammatory indomethacin did attenuate C5a Thus, similar B4 dependent independent cyclo-oxygenation arachidonic acid. Taken together, these data structurally diverse PMNL-chemotactic produce novel mechanism, involving PMNL-derived factors.