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

Francesco Boato12, Karen Rosenberger3, Sofie Nelissen1, Lies Geboes1, Eva M Peters45, Robert Nitsch6 and Sven Hendrix1*

Author Affiliations

1 Department of Morphology & BIOMED Institute, Campus Diepenbeek, Hasselt University, Agoralaan Gebouw C, Diepenbeek, BE 3590, Belgium

2 Present Address: Université Pierre et Marie Curie, Institut de la Vision, 17 rue Moreau, Paris, 75012, France

3 Department of Neurology, Charité Universitätsmedizin, Charitéplatz 1, Berlin, D-10117, Germany

4 Psychoneuroimmunology, University-Medicine Charité, Charité Center 12 for Internal Medicine and Dermatology, Berlin, D-10117, Germany

5 Department of Psychosomatic Medicine, Justus-Liebig-University, Klinikstrasse 32, D-35392, Gießen, Germany

6 Institute of Microanatomy and Neurobiology, University Medical Center, Johannes Gutenberg University, Langenbeckstrasse 1, 55131, Mainz, Germany

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Journal of Neuroinflammation 2013, 10:6  doi:10.1186/1742-2094-10-6

Published: 14 January 2013


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

IL-1β; Corticospinal tract; Glial scar; Spinal cord compression injury