Interleukin-1 enhances pain reflexes. Mediation through increased prostaglandin E2 levels.
Interleukin-1 (IL-1) has been shown to induce inflammatory reactions in part through increased prostaglandin production. Prostaglandins of the E- and I-type sensitize nociceptors in peripheral tissues. We have therefore investigated the effect of IL-1 perfusion in the isolated rabbit ear, a model which allows the assessment of peripheral pain. Natural IL-1 from human monocytes, IL-1 from glioblastoma cells as well as recombinant IL-1 alpha or beta, increased the pain reflex induced by acetylcholine in a concentration dependent manner. The PGE2 levels were measured in the perfusate and were found to be enhanced more than 10-fold after the infusion of IL-1 alpha or IL-1 beta. This effect was paralleled by the enhanced pain reflexes and persisted for at least one hour after cessation of the IL-1 perfusion. Both the increased pain reflexes as well as the enhanced PGE2 levels were abolished by addition of the cyclooxygenase inhibitor diclofenac-Na (Voltaren) to the perfusion fluid. These results show that besides the numerous known physiological functions of IL-1, it may also play a role in peripheral pain sensations.
Schweizer
A
A
Research Department, CIBA-GEIGY Ltd., Basel, Switzerland.
Feige
U
U
Fontana
A
A
Müller
K
K
Dinarello
C A
CA
D000818:Animals; D015232:Dinoprostone / Q000378:metabolism* / Q000494:pharmacology; D004423:Ear; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D011817:Rabbits; D011994:Recombinant Proteins / Q000494:pharmacology
D007375:Interleukin-1; D011994:Recombinant Proteins; D015232:Dinoprostone