Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats

Abstract

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.

Preferential and Bidirectional Labeling of the Rubrospinal Tract with Adenovirus-GFP for Monitoring Normal and Injured Axons

“…Contusive and hemi-contusive SCI was performed using a New York University (NYU) impactor, as described previously (Gensel et al, 2006;Wang et al, 2006). Lateral hemisection was carried out with a pair of iridectomy scissors as described previously (Arvanian et al, 2009).…”

“…After appropriate survival, the rats were perfused and the spinal cords and brains were removed, cryo-protected, and sectioned as described previously (Sivasankaran et al, 2004;Wang et al, 2006). To ensure that all FG-labeled neurons in the brain were available for visualization, the entire brain was serially sectioned transversely at 20 lm from the medulla to the motor cortex.…”

Molecular insights of the injured lesions of rat spinal cords: Inflammation, apoptosis, and cell survival

“…In our study, we made several additional advances to broaden our understanding of SCI-induced gene expression changes, specially concentrated in identification of molecular cell death and regeneration mechanism which occur during acute phase of injury. A large amount of research relevant to basic science, pathology, and novel pharmacological strategies can clearly be expected from differentially expressed transcript and protein studies of the injured spinal cord [14,31,32]. Additionally, further genomic analysis will be needed to focus on specific genes' identification overexpressed in injured spinal cord tissues.…”

A possible role for sPLA2 in oligodendrocyte death and spinal cord injury.

“…In the presence of 15-lipoxygenase the addition of sPLA 2 -IIA or IB greatly enhances the accumulation of hydroperoxides of oxidized free fatty acids (Neuzil et al, 1998). Finally, it can be assumed that the proinflammatory effects of sPLA 2 would result in an immigration of immune cells, which will release copious amounts of ROS (Blight, 1985, Popovich et al, 1997, Park et al, 2004, Jones et al, 2005a, Fleming et al, 2006, Wang et al, 2006. For a review of the ROS species produced by the enzymatic effects of sPLA 2 please see (Nanda et al, 2007).…”

“…Following SCI, inflammatory cells such as polymorphonuclear neutrophils, macrophages, and lymphocytes quickly infiltrate into the traumatized cord, and flood the interstitial tissue with proinflammatory cytokines such as TNF-α and IL-1β, and neurotoxic factors from leukocytes such as nitric oxide, hydrogen peroxide, and myeloperoxidase (Blight, 1985, Popovich et al, 1997, Park et al, 2004, Jones et al, 2005a, Fleming et al, 2006, Wang et al, 2006. Free radical generation and lipid peroxidation were also found to be early events subsequent to SCI (Hall and Braughler, 1986, Hall et al, 1992.…”