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Title:
Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats | Acta Neuropathologica
Description:
Post-traumatic inflammation response has been implicated in secondary injury mechanisms after spinal cord injury (SCI). Interleukin-1 (IL-1) is a key inflammatory mediator that is increasingly expressed after SCI. The action of IL-1 is mediated through its functional receptor, type I interleukin-1 receptor (IL-1RI). However, whether this receptor is expressed after SCI remains to be elucidated. In the present study, the temporospatial expression of IL-1RI was detected in rats that received a moderate contusive SCI (a 10 g rod dropped at a height of 12.5 mm) at the ninth to tenth thoracic vertebral level using a widely used New York University impact device. Our study demonstrated that IL-1RI was slightly increased at 4 h post-injury compared to the normal or sham-operated controls, reached the peak at 8 h at mRNA level (4.44-fold, P<0.01) and 1 d at protein level (2.62-fold, P<0.01). IL-1RI remained at its elevated levels for a relatively long duration (4 h–7 days). Spatially, IL-1RI was observed throughout the entire length of a 10 mm-long cord segment containing the injury epicenter. Colocalization of IL-1RI was found in neurons, oligodendrocytes, astrocytes, and activated microglia. Our results suggest that the elevated expression of IL-1RI after SCI may contribute to posttraumatic inflammation responses of IL-1.
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pubmed, google, scholar, cas, article, interleukin, spinal, cord, injury, receptor, type, brain, neurosci, expression, rat, interleukinbeta, inflammatory, ilri, res, research, traumatic, wang, access, rothwell, rats, sci, astrocytes, science, cytokines, privacy, cookies, content, adult, university, levison, factor, induction, necrosis, mice, data, publish, search, xiaoming, response, microglia, open, receptors, cell, activation, ilbeta,
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- Vitkovic L, Bockaert J, Jacque C (2000) “Inflammatory” cytokines: neuromodulators in normal brain?
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headline:Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats
description:Post-traumatic inflammation response has been implicated in secondary injury mechanisms after spinal cord injury (SCI). Interleukin-1 (IL-1) is a key inflammatory mediator that is increasingly expressed after SCI. The action of IL-1 is mediated through its functional receptor, type I interleukin-1 receptor (IL-1RI). However, whether this receptor is expressed after SCI remains to be elucidated. In the present study, the temporospatial expression of IL-1RI was detected in rats that received a moderate contusive SCI (a 10 g rod dropped at a height of 12.5 mm) at the ninth to tenth thoracic vertebral level using a widely used New York University impact device. Our study demonstrated that IL-1RI was slightly increased at 4 h post-injury compared to the normal or sham-operated controls, reached the peak at 8 h at mRNA level (4.44-fold, P<0.01) and 1 d at protein level (2.62-fold, P<0.01). IL-1RI remained at its elevated levels for a relatively long duration (4 h–7 days). Spatially, IL-1RI was observed throughout the entire length of a 10 mm-long cord segment containing the injury epicenter. Colocalization of IL-1RI was found in neurons, oligodendrocytes, astrocytes, and activated microglia. Our results suggest that the elevated expression of IL-1RI after SCI may contribute to posttraumatic inflammation responses of IL-1.
datePublished:2006-02-03T00:00:00Z
dateModified:2006-02-03T00:00:00Z
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Inflammation
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IL-1
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headline:Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats
description:Post-traumatic inflammation response has been implicated in secondary injury mechanisms after spinal cord injury (SCI). Interleukin-1 (IL-1) is a key inflammatory mediator that is increasingly expressed after SCI. The action of IL-1 is mediated through its functional receptor, type I interleukin-1 receptor (IL-1RI). However, whether this receptor is expressed after SCI remains to be elucidated. In the present study, the temporospatial expression of IL-1RI was detected in rats that received a moderate contusive SCI (a 10 g rod dropped at a height of 12.5 mm) at the ninth to tenth thoracic vertebral level using a widely used New York University impact device. Our study demonstrated that IL-1RI was slightly increased at 4 h post-injury compared to the normal or sham-operated controls, reached the peak at 8 h at mRNA level (4.44-fold, P<0.01) and 1 d at protein level (2.62-fold, P<0.01). IL-1RI remained at its elevated levels for a relatively long duration (4 h–7 days). Spatially, IL-1RI was observed throughout the entire length of a 10 mm-long cord segment containing the injury epicenter. Colocalization of IL-1RI was found in neurons, oligodendrocytes, astrocytes, and activated microglia. Our results suggest that the elevated expression of IL-1RI after SCI may contribute to posttraumatic inflammation responses of IL-1.
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