• Aihui Li, Lixing Lao, Yi Wang, Haiqing Zhang, Ke Ren, Brian M Berman, and Ruixin Zhang.
• Center for Integrative Medicine, School of Medicine, Department of Biomedical Sciences, University of Maryland, Baltimore, Maryland 21201, USA.
• Neuroreport. 2007 Mar 26; 18 (5): 495-8.

AbstractIt is known that interleukin-1beta facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1beta 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-1ra, 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-1beta 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-1ra inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1beta facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression.

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