Interleukin-Ira inhibits Fos expression and hyperalgesia in rats

It is known that interleukin-1 beta facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1 beta in the expression of Fos, a marker of neuronal activation, and hyperalgesia caused by injecting complete Freund's adjuvant into one hind paw of the rat. Interleukin-receptor antagonist (interleukin-Ira, 0.005 mg/rat) was given intrathecally twice, 24 h before complete Freund's adjuvant and immediately before complete Freund's adjuvant injection, to block interleukin-1 beta action. Fos expression was measured 2 h after complete Freund's adjuvant injection. Paw withdrawal latency was used to assess hyperalgesia. The findings were that interleukin-Ira inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1 beta facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression.