Intraspinal injection of
quisqualic acid (QUIS) produces excitotoxic injury with pathological characteristics similar to those associated with ischemic and traumatic
spinal cord injury (SCI). Inflammatory responses appear to be a major component of the secondary neuronal injury initiated by SCI and play a role in the pathogenesis of QUIS-induced injury.
IL-10 is a potent antiinflammatory
cytokine that has been shown to reduce
inflammation and improve functional outcome in human and animal models of inflammatory diseases. We propose the administration of
IL-10 following excitotoxic SCI will attenuate the inflammatory response, thus resulting in increased neuronal survival. Female, Sprague-Dawley rats were given
intraspinal injections of QUIS followed by either intraspinal (5 ng, n = 8) or systemic
injections (5 microgram n = 14) of
IL-10. Survival times were varied (2-3 days) in order to produce a range of injury states and inflammatory involvement. When administered intraspinally,
IL-10 significantly exacerbated the QUIS damage (P < 0.05), resulting in an 11.2% increase in lesion volume. When given systemically,
IL-10 significantly decreased lesion volume by 18.1% in the more advanced injury (P < 0.05), but did not effect the more acute injury. These divergent effects were attributed to the modest inflammatory response in the short-term injury compared to the more robust inflammatory response in the more chronic injury. In conclusion, reducing the inflammatory response to SCI by systemic administration of
IL-10 resulted in a significant reduction in neuronal damage, suggesting that targeting injury-induced
inflammation may be an effective treatment strategy for acute SCI.