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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Interleukin-1 involvement in the induction of leukemia inhibitory factor mRNA expression following axotomy of sympathetic ganglia.
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Interleukin-1 involvement in the induction of leukemia inhibitory factor mRNA expression following axotomy of sympathetic ganglia.

机译：白细胞介素1参与交感神经节切开术后的白血病抑制因子mRNA表达的诱导。

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摘要

Axotomy of superior cervical (sympathetic) ganglia (SCG) results in increased neuropeptide gene expression. In vitro, neuropeptide gene expression is similarly increased by exposure to the inflammatory cytokine interleukin-1 (IL-1). The effect of IL-1 in-vitro has been shown to be mediated by leukemia inhibitory factor (LIF). Since IL-1 regulates neuropeptide expression via LIF in vitro, we asked whether axotomy in vivo produces an increase in LIF mRNA, and whether that increase is regulated by IL-1 activity. Within 6 h following axotomy, ganglionic LIF mRNA is substantially elevated. Moreover, axotomy produces a rapid and transient increase in intraganglionic IL-1 beta mRNA, followed rapidly by an increase in ICAM-1 mRNA, thereby suggesting a local source of IL-1 activity. Pretreatment with the anti-inflammatory agent dexamethasone (DEX) reduces the increases of both IL-1 beta and LIF mRNAs following axotomy. mRNA encoding the specific signal-transducing Type I IL-1 receptor is present in unlesioned SCG in vivo, and increases following axotomy. Local application of IL-1 beta in vivo induces LIF mRNA even in uninjured ganglia, though not to the extent seen with axotomy. DEX treatment blocks this IL-1 beta-mediated increase in LIF mRNA. Therefore, DEX blocks the induction of LIF mRNA by inhibiting both the production of IL-1 and its action on LIF gene expression. Axotomy of a homozygous IL-1 receptor type I gene knockout mouse leads to a delayed and/or diminished induction of LIF mRNA in SCG, but does not prevent LIF mRNA expression. We conclude that while IL-1 is likely to be involved in the cascade of gene expression that follows axotomy, it alone is not sufficient to mediate the full induction of LIF mRNA by axotomy.
机译：上颈（交感神经）神经节（SCG）的轴切术导致神经肽基因表达增加。在体外，通过暴露于炎性细胞因子白介素-1（IL-1），神经肽基因表达也会类似地增加。已经显示IL-1的体外作用是由白血病抑制因子（LIF）介导的。由于IL-1在体外通过LIF调节神经肽的表达，因此我们询问了体内轴切术是否会导致LIF mRNA的增加，以及这种增加是否受IL-1活性的调节。切开后6小时内，神经节LIF mRNA显着升高。此外，轴切术使神经节内IL-1βmRNA迅速而短暂地增加，随后迅速使ICAM-1 mRNA增加，从而提示IL-1活性的局部来源。用抗炎药地塞米松（DEX）预处理可减少轴切术后的IL-1β和LIF mRNA的增加。编码特异性信号传导I型IL-1受体的mRNA存在于体内未损伤的SCG中，并在切开后增加。 IL-1β在体内的局部应用即使在未受伤的神经节中也能诱导LIF mRNA的表达，尽管在轴切术中没有达到这种程度。 DEX处理可阻止这种IL-1β介导的LIF mRNA的增加。因此，DEX通过抑制IL-1的产生及其对LIF基因表达的作用来阻止LIF mRNA的诱导。对纯合的IL-1受体I型基因敲除小鼠进行轴突切开可导致SCG中LIF mRNA的诱导延迟和/或减弱，但不会阻止LIF mRNA表达。我们得出的结论是，尽管IL-1可能参与了轴切术之后基因表达的级联，但仅靠IL-1不足以介导轴切术对LIF mRNA的完全诱导。

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