Absence of IL-1[beta] positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury

• Published in: Journal of neuroinflammation 2013-01, Vol.10 (1), p.6-6
• Main Authors: Boato, Francesco, Rosenberger, Karen, Nelissen, Sofie, Geboes, Lies, Peters, Eva M, Nitsch, Robert, Hendrix, Sven
• Format: Article
• Language: English
• Subjects: Analysis; Animal models; Apoptosis; Axonogenesis; Axons; Brain slice preparation; Central nervous system; Compression; Cytokines; Drug dosages; Experiments; Fibers; Glia; Gliosis; Immune system; Inflammation; Laboratory animals; Medical research; Medicine, Experimental; Mortality; Nervous system; Neurodegeneration; Neuroprotection; Neurosciences; Neurotoxicity; Physiological aspects; Plasticity (axonal); Plasticity (developmental); Plasticity (functional); Plasticity (glial); Plasticity (spinal); Pyramidal tracts; Recovery of function; Regeneration; Rodents; Spinal cord injuries; Spinal cord injury; Studies; Substantia alba
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/1742-2094-10-6

Precise crosstalk between the nervous and immune systems is important for neuroprotection and axon plasticity after injury. Recently, we demonstrated that IL-1[beta] acts as a potent inducer of neurite outgrowth from organotypic brain slices in vitro, suggesting a potential function of IL-1[beta] in axonal plasticity. Here, we have investigated the effects of IL-1[beta] 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[beta] deficiency model (IL-1[beta]KO mice) and administered recombinant IL-1[beta]. 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[beta]. Consistently, the treatment significantly worsened the neurological outcome after SCI in mice compared with PBS controls. In contrast, the absence of IL-1[beta] in IL-1[beta]KO 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[beta]KO mice relative to controls. Our study for the first time characterizes the detrimental effects of IL-1[beta] not only on lesion development (in terms of size and glia activation), but also on the plasticity of central nervous system axons after injury.