Absence of IL-1β positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury.
Absence of IL-1β positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury.
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DOI:
10.1186/1742-2094-10-6
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发表时间:
2013-01-14
影响因子:
9.3
通讯作者:
Hendrix S
中科院分区:
文献类型:
--
作者:
Boato F;Rosenberger K;Nelissen S;Geboes L;Peters EM;Nitsch R;Hendrix S
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.
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影响因子:
4.2
作者:
Edoff, K;Jerregård, H
通讯作者:
Jerregård, H
影响因子:
9.3
作者:
Sato A;Ohtaki H;Tsumuraya T;Song D;Ohara K;Asano M;Iwakura Y;Atsumi T;Shioda S
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Shioda S
影响因子:
5.3
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通讯作者:
Allan, Stuart M.
影响因子:
2.9
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通讯作者:
McAdoo, David J.
影响因子:
14.5
作者:
Perrin, FE;Lacroix, S;David, S
通讯作者:
David, S