Tumour necrosis factor- α mediates carrageenin-induced knee-joint incapacitation and also triggers overt nociception in previously inflamed rat knee-joints

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Abstract
Tense and long-lasting (>8 h) peaking incapacitation response. TNFα injected in naive joints did not elicit incapacitation. Anti-TNFα serum in situ treatment specifically inhibited CG-induced incapacitation in naive joints, and also TNFα-induced incapacitation in primed joints. Hoe-140 (d-Arg0[Hyp3,Thi5,d-Tic7,Oic8]-bradykinin, a bradykinin B2 receptor antagonist, given before CG, abolished incapacitation, but was without effect when injected 3 h after. Hoe-140 given before or after the CG injection in primed joints was without effect, but it produced a partial inhibitory effect in the early phase (1 h) of TNFα-induced incapacitation. Des-Arg9[Leu8]bradykinin, a bradykinin B1 receptor antagonist, given intra-articularly after CG or TNFα, reversed incapacitation either in naive or primed joints. Indomethacin abolished the incapacitation induced by CG in naive joints, but only the 5-lipoxygenase inhibitor MK-886 plus indomethacin blocked the response in primed joints. MK-886 did not modify CG-induced incapacitation in naive joints, but lately reversed CG-induced incapacitation in primed joints, and blocked TNFα-induced response. Substance P or prostaglandin E2 did not induce incapacitation in either naive or primed joints. Our results support the conclusion that TNFα is a mediator of CG-induced inflammatory incapacitation, and is able to induce the further release of kinins and leukotrienes, which is suggested to have an important role in the maintenance of long-lasting nociceptive response....

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