Effects of interleukin-10 (IL-10) on pain behavior and gene expression following excitotoxic spinal cord injury in the rat

Jeffery A. Plunkett, Chen Guang Yu, Julia M. Easton, John R. Bethea, Robert P. Yezierski

Research output: Contribution to journalArticlepeer-review

149 Scopus citations


Intraspinal injection of quisqualic acid (QUIS) produces excitotoxic injury with pathophysiological characteristics similar to those associated with ischemic and traumatic spinal cord injury (SCI). Responses to QUIS-induced injury include an inflammatory component, as well as the development of spontaneous and evoked pain behaviors. We hypothesized that QUIS-induced inflammation and subsequent gene expression contribute to the development and progression of pain-related behaviors and that blockade of inflammation-related gene expression leads to the amelioration of these behaviors. Using the QUIS model of spinal cord injury, we examined whether interleukin-10 (IL-10), a potent anti-inflammatory cytokine, is able to reduce mRNA levels of inflammatory and cell death-related genes leading to a reduction of pain behaviors. The results demonstrate that animals receiving systemic injection of IL-10, 30 minutes following QUIS-induced SCI, showed a significant delay in the onset of excessive grooming behavior, a significant reduction in grooming severity, and a significant reduction in the longitudinal extent of a pattern of neuronal loss within the spinal cord characterized as "grooming-type damage." QUIS injections also resulted in an increase in mRNA levels of interleukin-1 beta (IL-1β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), CD95 ligand (CD95-L, also called FAS-L/APO-1L), and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Results of QUIS injury plus IL-10 treatment resulted in a significant downregulation of IL1-β and iNOS mRNA and these results were supported by Western blot analysis of protein levels following IL-10 treatment. These data suggest that IL-10 reduces inflammation and that targeting injury-induced inflammation is an effective strategy for limiting the extent of neuronal damage following excitotoxic SCI and thus the onset and progression of injury-induced pain behaviors.

Original languageEnglish
Pages (from-to)144-154
Number of pages11
JournalExperimental Neurology
Issue number1
StatePublished - 2001

Bibliographical note

Funding Information:
This work was supported by The Hollfelder Foundation, The Miami Project Appropriation No. 207, Lois Pope LIFE Fellowship (J.A.P.), NIH Neuroscience Training Grant, University of Miami School of Medicine (J.A.P.), Paralyzed Veterans of America, SCRF No. 2051 (J.A.P.), National Institutes of Health Grants NS 37130 (J.R.B.), and NS 40096 (R.P.Y.). We also acknowledge the expert technical support of Linda Danials, Gladys Ruenes, Dimarys Sanchez, and Robert Camerena.

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience


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