Intrathecal administration of IL-1ra (20 ng) on days 0 to 3 post-surgery also facilitated the CCI-induced development of mechanical allodynia, and this early developed pain was dose-dependently attenuated by the administration of the P450c17 inhibitor, ketoconazole (1, 3, or 10 nmol) or the astrocyte metabolic inhibitor, fluorocitrate (0.01, 0.03, or 0.1 nmol).
Correlation between pain reduction and changes to MMP-9 after 8 weeks was highly significant (<i>P</i><0.01), whereas correlation between pain reduction and changes to IL-1ra reached significance at 2 weeks for the group consuming 3 caps once daily (<i>p</i><0.04).
If present in high enough concentrations, IL-1-Ra has the potential to inhibit Interleukin-1, the chief offender that promotes the pro-inflammatory cascade causing pain, swelling and joint dysfunction associated with osteoarthritis (OA).
The result showed that patients with the IL1A T allele, in combination with the IL1RN A allele had more pain and a slower recovery than other patients (VAS p = 0.049, ODI p = 0.059 rmANOVA; VAS p = 0.003, ODI p = 0.050 one-way ANOVA at 12 months).
Polymorphisms in interleukin 1 (IL-1) family of genes (IL1A, IL1B) and in IL-1 receptor antagonist (IL-1Ra, coded by IL1RN) may therefore induce alterations in cytokine levels/effects and pain related response.
The present study examined the hypothesis that polymorphism of IL-1beta and IL-1Ra genes is involved in pain sensitivity and morphine consumption in the immediate postoperative period.
A role for proinflammatory cytokines and fractalkine in analgesia, tolerance, and subsequent pain facilitation induced by chronic intrathecal morphine.
The expression levels of the cytokine-mRNAs were inversely correlated with the degree of pain (IL-1beta: r = 0.930; secreted IL-1ra: r = 0.861; intracellular IL-1ra: r = 0.932, P < 0.001 respectively).
The results of the current study showed intraarticular expression of interleukin-1 receptor antagonist to have favorable effects such as an approximately 28 day upregulation of interleukin-1 receptor antagonist protein expression, significant improvement in clinical parameters of pain and disease activity, and beneficial effects in histologic parameters measured from synovial membrane and articular cartilage when compared with nontransduced joints.