title: Absence of IL-1β positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury.
abstract: 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.
authors: Department of Morphology & BIOMED Institute, Campus Diepenbeek, Hasselt University, Agoralaan Gebouw C, Diepenbeek, BE 3590, Belgium.
authors: Francesco
authors: F
authors: Boato
authors: Karen
authors: K
authors: Rosenberger
authors: Sofie
authors: S
authors: Nelissen
authors: Lies
authors: L
authors: Geboes
authors: Eva M
authors: EM
authors: Peters
authors: Robert
authors: R
authors: Nitsch
authors: Sven
authors: S
authors: Hendrix
mesh_terms: D000818:Animals; D001369:Axons / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D005260:Female; D005911:Gliosis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D053583:Interleukin-1beta / Q000172:deficiency* / Q000633:toxicity; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009416:Nerve Regeneration / Q000187:drug effects / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D011994:Recombinant Proteins / Q000633:toxicity; D013119:Spinal Cord Injuries / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D016896:Treatment Outcome
chemical_list: D053583:Interleukin-1beta; D011994:Recombinant Proteins