%0 Journal Article %T Absence of IL-1¦Â positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury %A Boato Francesco %A Rosenberger Karen %A Nelissen Sofie %A Geboes Lies %J Journal of Neuroinflammation %D 2013 %I BioMed Central %R 10.1186/1742-2094-10-6 %X Precise crosstalk between the nervous and immune systems is important for neuroprotection and axon plasticity after injury. Recently, we demonstrated that IL-1¦Â acts as a potent inducer of neurite outgrowth from organotypic brain slices in vitro, suggesting a potential function of IL-1¦Â in axonal plasticity. Here, we have investigated the effects of IL-1¦Â 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-1¦Â deficiency model (IL-1¦ÂKO mice) and administered recombinant IL-1¦Â. 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-1¦Â. Consistently, the treatment significantly worsened the neurological outcome after SCI in mice compared with PBS controls. In contrast, the absence of IL-1¦Â in IL-1¦ÂKO 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-1¦ÂKO mice relative to controls. Our study for the first time characterizes the detrimental effects of IL-1¦Â not only on lesion development (in terms of size and glia activation), but also on the plasticity of central nervous system axons after injury. %K IL-1¦Â %K Corticospinal tract %K Glial scar %K Spinal cord compression injury %U http://www.jneuroinflammation.com/content/10/1/6