| First Author | Boato F | Year | 2013 |
| Journal | J Neuroinflammation | Volume | 10 |
| Pages | 6 | PubMed ID | 23317037 |
| Mgi Jnum | J:319017 | Mgi Id | MGI:6862353 |
| Doi | 10.1186/1742-2094-10-6 | Citation | Boato F, et al. (2013) Absence of IL-1beta positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury. J Neuroinflammation 10:6 |
| abstractText | Precise crosstalk between the nervous and immune systems is important for neuroprotection and axon plasticity after injury. Recently, we demonstrated that IL-1beta acts as a potent inducer of neurite outgrowth from organotypic brain slices in vitro, suggesting a potential function of IL-1beta in axonal plasticity. Here, we have investigated the effects of IL-1beta on axon plasticity during glial scar formation and on functional recovery in a mouse model of spinal cord compression injury (SCI). We used an IL-1beta deficiency model (IL-1betaKO mice) and administered recombinant IL-1beta. In contrast to our hypothesis, the histological analysis revealed a significantly increased lesion width and a reduced number of corticospinal tract fibers caudal to the lesion center after local application of recombinant IL-1beta. Consistently, the treatment significantly worsened the neurological outcome after SCI in mice compared with PBS controls. In contrast, the absence of IL-1beta in IL-1betaKO mice significantly improved recovery from SCI compared with wildtype mice. Histological analysis revealed a smaller lesion size, reduced lesion width and greatly decreased astrogliosis in the white matter, while the number of corticospinal tract fibers increased significantly 5 mm caudal to the lesion in IL-1betaKO mice relative to controls. Our study for the first time characterizes the detrimental effects of IL-1beta not only on lesion development (in terms of size and glia activation), but also on the plasticity of central nervous system axons after injury. |
