Interleukin-8 as a mediator of sympathetic pain
Department of Endocrinology, National Institute for Biological Standards and Control, Blanche Lane, South Mimms, Potters Bar, Herts. EN6 3QG
- 1The hyperalgesic effects of interleukin-8 (IL-8), interleukin-1β (IL-1β) and carrageenin were measured in a rat paw pressure test.
- 2IL-8 evoked a dose-dependent hyperalgesia which was attenuated by a specific antiserum, the β-adrenoceptor antagonists atenolol and propranolol, the dopamine1 receptor antagonist SCH 23390 and the adrenergic neurone-blocking agent guanethidine. The hyperalgesia was not attenuated by the cyclo-oxygenase inhibitor indomethacin or the IL-1β analogue Lys-d-Pro-Thr.
- 3IL-1β-evoked hyperalgesia was attenuated by indomethacin and Lys-d-Pro-Thr but not by atenolol or SCH 23390.
- 4Carrageenin-evoked hyperalgesia was attenuated by atenolol, indomethacin and anti-IL-8 serum. The effects of atenolol and anti-IL-8 serum were not additive. The effects of indomethacin and anti-IL-8 serum were additive: this combination abolished carrageenin-evoked hyperalgesia.
- 5A new biological activity of IL-8 is described, namely the capacity to evoke hyperalgesia by a prostaglandin-independent mechanism. IL-8 is the first endogenous mediator to be identified as evoking hyperalgesia involving the sympathetic nervous system. Since IL-8 is released by activated macrophages and endothelial cells it may be a humoral link between tissue injury and sympathetic hyperalgesia.