Interleukin‐8 as a mediator of sympathetic pain

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Abstract
1 The hyperalgesic effects of interleukin-8 (IL-8), interleukin-1β (IL-1β) and carrageenin were measured in a rat paw pressure test. 2 IL-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. 3 IL-1β-evoked hyperalgesia was attenuated by indomethacin and Lys-d-Pro-Thr but not by atenolol or SCH 23390. 4 Carrageenin-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. 5 A 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.