Source:http://linkedlifedata.com/resource/pubmed/id/15026134
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2004-3-17
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| pubmed:abstractText |
Interleukin-10 (IL-10) has been utilized as a neuroprotective agent in experimental models of spinal cord injury because of its potent anti-inflammatory properties. Previous studies have delivered a single dose (5 microg) of IL-10 following experimental spinal cord injury in the rat, and demonstrated various degrees of neuroprotection. However, the role of endogenous production of IL-10 has not been considered. Therefore, the purpose of the current study was to establish the role of endogenous IL-10 and demonstrate the true potential of exogenous IL-10 administration through the use of IL-10((-/-)) mice. Using the quisqualic acid model of spinal cord injury, we examined the extent of gray matter damage and onset of injury-induced pain behaviors at various time points following injury in wild-type vs. IL-10((-/-)) mice. Additionally, IL-10 was reconstituted in IL-10 deficient mice by the intraperitoneal administration of 50 ng recombinant murine (rm) IL-10 30 min following quisqualic acid injection. Animals were observed daily following injury for the onset of pain-behaviors. At days 1, 7, and 14 following injection, lesion analysis revealed a greater extent of damage at early time points (1 day, 7 days) following injury in the IL-10((-/-)) animals as compared with wild-type animals. However, by 14 days post-experimental spinal cord injury, the extent of damage between the two groups was not significant. IL-10((-/-)) animals that received the single (50 ng) rmIL-10 injection following injury displayed gray matter damage patterns similar to wild-type animals. The pronounced early damage noted in the IL-10((-/-)) animals was associated with an approximately two-fold increase in peripheral neutrophils, an index of an innate immune response to injury, compared with wild-type mice. In addition, wild type and IL-10((-/-)) animals receiving rmIL-10 demonstrated a delay in the onset of injury-induced pain behaviors. However, by 14 days post-experimental spinal cord injury the overall incidence of pain behaviors was similar between all treatment groups. Therefore, the absence of IL-10 expression accelerates the kinetics of lesion expansion, the onset of pain behaviors, and the peripheral immune response to spinal cord injury. Endogenous IL-10 and low doses of exogenous IL-10 are neuroprotective at 1 and 7 days following injury. Therefore, the results of the current study suggest that low dose IL-10 administration acutely following spinal cord injury has potential as a therapeutic agent for limiting tissue loss following injury.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0306-4522
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
124
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
945-52
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| pubmed:meshHeading |
pubmed-meshheading:15026134-Animals,
pubmed-meshheading:15026134-Behavior, Animal,
pubmed-meshheading:15026134-Blood Cell Count,
pubmed-meshheading:15026134-Interleukin-10,
pubmed-meshheading:15026134-Male,
pubmed-meshheading:15026134-Mice,
pubmed-meshheading:15026134-Mice, Inbred C57BL,
pubmed-meshheading:15026134-Mice, Knockout,
pubmed-meshheading:15026134-Neuroprotective Agents,
pubmed-meshheading:15026134-Neurotoxins,
pubmed-meshheading:15026134-Pain,
pubmed-meshheading:15026134-Periaqueductal Gray,
pubmed-meshheading:15026134-Spinal Cord Diseases
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| pubmed:year |
2004
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| pubmed:articleTitle |
The effects of endogenous interleukin-10 on gray matter damage and the development of pain behaviors following excitotoxic spinal cord injury in the mouse.
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| pubmed:affiliation |
Division of Physical Therapy, Shenandoah University, 333 West Cork Street, Winchester, VA 22601, USA. kabraham@su.edu
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| pubmed:publicationType |
Journal Article
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