Dept. of Functional Morphology & BIOMED Institute, Hasselt University, Belgium.
J Neuroinflammation. 2011 Dec 26;8:183. doi: 10.1186/1742-2094-8-183.
Pro-inflammatory cytokines such as interleukin-1 beta (IL-1β) are considered to exert detrimental effects during brain trauma and in neurodegenerative disorders. Consistently, it has been demonstrated that IL-1β suppresses neurotrophin-mediated neuronal cell survival rendering neurons vulnerable to degeneration. Since neurotrophins are also well known to strongly influence axonal plasticity, we investigated here whether IL-1β has a similar negative impact on neurite growth. We analyzed neurite density and length of organotypic brain and spinal cord slice cultures under the influence of the neurotrophins NGF, BDNF, NT-3 and NT-4. In brain slices, only NT-3 significantly promoted neurite density and length. Surprisingly, a similar increase of neurite growth was induced by IL-1β. Additionally, both factors increased the number of brain slices displaying maximal neurite growth. Furthermore, the co-administration of IL-1β and NT-3 significantly increased the number of brain slices displaying maximal neurite growth compared to single treatments. These data indicate that these two factors synergistically stimulate two distinct aspects of neurite outgrowth, namely neurite density and neurite length from acute organotypic brain slices.
促炎细胞因子，如白细胞介素-1β（IL-1β），被认为在脑外伤和神经退行性疾病中发挥有害作用。一致地，已经证明 IL-1β抑制神经营养因子介导的神经元细胞存活，使神经元易发生退化。由于神经营养因子也被广泛认为强烈影响轴突可塑性，我们在这里研究了 IL-1β是否对轴突生长有类似的负面影响。我们分析了在神经营养因子 NGF、BDNF、NT-3 和 NT-4 的影响下，器官型脑和脊髓切片培养物中的神经突密度和长度。在脑切片中，只有 NT-3 显著促进了神经突密度和长度的增加。令人惊讶的是，IL-1β也诱导了类似的轴突生长增加。此外，这两种因子都增加了显示最大神经突生长的脑切片数量。此外，与单独处理相比，IL-1β 和 NT-3 的共同给药显著增加了显示最大神经突生长的脑切片数量。这些数据表明，这两种因子协同刺激神经突生长的两个不同方面，即急性器官型脑切片的神经突密度和神经突长度。
