Spinal interleukin-1 β reduces inflammatory pain

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Abstract
N the modulation of pain transmission in both the peripheral and central nervous systems. We evaluated the spinal effect of this cytokine in the presence and absence of a peripheral carrageenan inflammation in rats since the spinal cord is a major region of the central nervous system in which nociceptive input is processed and modulated. Our results indicate that intrathecal IL-1β has no effect on the latency of paw withdrawal in response to a noxious thermal stimuluation in normal rats. In contrast, we have observed that IL-1β produces significant antinociception when administered intrathecally in rats with peripheral inflammation (carrageenan model). The IL-1β effect appears to be selective as it is reversed when IL-1β is administered in the presence of an IL-1β neutralizing antibody. We evaluated some putative mechanisms of this IL-1β-mediated antinociception and found it to be non-opioid-dependent. Collectively, these data indicate that intrathecal IL-1β has no effect on the processing of thermal nociceptive information in the absence of a peripheral inflammation. Therefore, the response to acute pain remains normal in these rats. In contrast, IL-1β is antinociceptive when applied spinally during inflammation. These results indicate that IL-1β reduces inflammatory hyperalgesia while sparing the protective functions of acute pain. This study offers new insights into the role of IL-1β and nociceptive processing at the level of the spinal cord and suggests that development of IL-1β agonists may be an alternative to opiate based therapies in the treatment of inflammatory pain....