Article date: November 1991
By: F.Q. Cunha, B.B. Lorenzetti, S. Poole, S.H. Ferreira, in Volume 104, Issue 3, pages 765-767
The hyperalgesic effects of interleukin‐8 (IL‐8), interleukin‐1β (IL‐1β) and carrageenin were measured in a rat paw pressure test.
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.
IL‐1β‐evoked hyperalgesia was attenuated by indomethacin and Lys‐d‐Pro‐Thr but not by atenolol or SCH 23390.
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.
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.
The hyperalgesic effects of interleukin‐8 (IL‐8), interleukin‐1β (IL‐1β) and carrageenin were measured in a rat paw pressure test.
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.
IL‐1β‐evoked hyperalgesia was attenuated by indomethacin and Lys‐d‐Pro‐Thr but not by atenolol or SCH 23390.
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.
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.
DOI: 10.1111/j.1476-5381.1991.tb12502.x
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