Lipocalin 2 (LCN2), an immunomodulator, regulates various cellular processes such as iron transport and defense against bacterial infection. Under pathological conditions, LCN2 promotes neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes. Although it seems to have a negative influence on the functional outcome in spinal cord injury (SCI), the extent of its involvement in SCI and the underlying mechanisms are not yet fully known. In this study, using a SCI contusion mouse model, we first investigated the expression pattern of Lcn2 in different parts of the CNS (spinal cord and brain) and in the liver and its concentration in blood serum. Interestingly, we could note a significant increase in LCN2 throughout the whole spinal cord, in the brain, liver, and blood serum. This demonstrates the diversity of its possible sites of action in SCI. Furthermore, genetic deficiency of Lcn2 (Lcn2^−/−) significantly reduced certain aspects of gliosis in the SCI-mice. Taken together, our studies provide first valuable hints, suggesting that LCN2 is involved in the local and systemic effects post SCI, and might modulate the impairment of different peripheral organs after injury.

Lipocalin 2 (LCN2) 是一种免疫调节剂，可调节各种细胞过程，例如铁转运和防御细菌感染。在病理条件下，LCN2 通过募集和激活免疫细胞和胶质细胞，特别是小胶质细胞和星形胶质细胞来促进神经炎症。尽管它似乎对脊髓损伤 (SCI) 的功能结果有负面影响，但它在 SCI 中的参与程度及其潜在机制尚不完全清楚。在这项研究中，我们使用 SCI 挫伤小鼠模型，首先研究了 Lcn2 在 CNS 不同部位（脊髓和大脑）和肝脏中的表达模式及其在血清中的浓度。有趣的是，我们可以注意到整个脊髓、大脑、肝脏和血清中的 LCN2 显着增加。这表明其在 SCI 中可能的作用部位的多样性。此外，Lcn2 的遗传缺陷（Lcn2^-/- ) 显着减少 SCI 小鼠神经胶质增生的某些方面。总之，我们的研究提供了第一个有价值的提示，表明 LCN2 参与 SCI 后的局部和全身效应，并可能调节损伤后不同外周器官的损伤。