Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal; ICVS/3B's - PT Government Associate Laboratory, Braga/Guimarães, Portugal.
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal; ICVS/3B's - PT Government Associate Laboratory, Braga/Guimarães, Portugal; Clinical Academic Center, Braga, Braga, Portugal.
J Neuroimmunol. 2022 Jul 15;368:577872. doi: 10.1016/j.jneuroim.2022.577872. Epub 2022 Apr 18.
The contribution of lipocalin-2 (LCN2) to multiple sclerosis (MS) is controversial. Herein, we induced experimental autoimmune encephalomyelitis (EAE) in LCN2-null and wild-type (Wt) mice. While we did not find differences between genotypes regarding clinical score, LCN2-null EAE mice presented decreased expression of interferon gamma and diminished demyelination in the cerebellum. Both genotypes presented similar alterations in the thymocyte and splenocyte populations. In MS patients, higher LCN2 CSF levels at diagnosis could be associated with faster disease progression, however further studies are needed to confirm these results, since this association was lost after controlling for the patients age, presence of oligoclonal bands and gender. Overall, our results support a harmful role for LCN2 in the disease context.
载脂蛋白 L2（LCN2）在多发性硬化症（MS）中的作用存在争议。在此，我们在 LCN2 缺失和野生型（Wt）小鼠中诱导实验性自身免疫性脑脊髓炎（EAE）。虽然我们没有发现基因型之间在临床评分方面存在差异，但 LCN2 缺失的 EAE 小鼠的干扰素γ表达降低，小脑脱髓鞘减少。两种基因型的胸腺细胞和脾细胞群体都有相似的改变。在 MS 患者中，诊断时 CSF 中更高的 LCN2 水平可能与疾病进展更快有关，然而，需要进一步的研究来证实这些结果，因为在控制患者年龄、寡克隆条带的存在和性别后，这种关联就消失了。总的来说，我们的结果支持 LCN2 在疾病背景下的有害作用。
