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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/14919

Title: Absence of IL-1 beta positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury
Authors: Boato, Francesco
Rosenberger, Karen
Nelissen, Sofie
Geboes, Lies
Peters, Eva M.
Nitsch, Robert
Hendrix, Sven
Issue Date: 2013
Citation: JOURNAL OF NEUROINFLAMMATION, 10 (Article 6), p. 1-11
Abstract: 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.
Notes: [Boato, Francesco; Nelissen, Sofie; Geboes, Lies; Hendrix, Sven] Hasselt Univ, Dept Morphol, BE-3590 Diepenbeek, Belgium. [Boato, Francesco; Nelissen, Sofie; Geboes, Lies; Hendrix, Sven] Hasselt Univ, BIOMED Inst, BE-3590 Diepenbeek, Belgium. [Rosenberger, Karen] Charite, Dept Neurol, D-10117 Berlin, Germany. [Peters, Eva M.] Charite, Charite Ctr Internal Med & Dermatol 12, D-10117 Berlin, Germany. [Peters, Eva M.] Univ Giessen, Dept Psychosomat Med, D-35392 Giessen, Germany. [Nitsch, Robert] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Microanat & Neurobiol, D-55131 Mainz, Germany.
URI: http://hdl.handle.net/1942/14919
DOI: 10.1186/1742-2094-10-6
ISI #: 000315719000001
ISSN: 1742-2094
Category: A1
Type: Journal Contribution
Validation: ecoom, 2014
Appears in Collections: Research publications

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