Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
The No.1 People's Hospital of Shizuishan, Shizuishan, 753200, Ningxia, China.
Sci Rep. 2023 May 23;13(1):8354. doi: 10.1038/s41598-023-35610-w.
Guillain-Barré syndrome (GBS) is an acute idiopathic polyneuropathy which is related to infection and immune mechanism. The exact pathogenesis of the disease is unknown and treatment is limited. Thus, the purpose of the study is to identify biomarkers of GBS serum and elucidate their involvement in the underlying pathogenesis of GBS that could help to treat GBS more accurately. Antibody array technology was used to detect the expression levels of 440 proteins in serum of 5 GBS group and 5 healthy control group. Sixty-seven differentially expressed proteins (DEPs) were identified by antibody array, among which FoLR1, Legumain, ErbB4, IL-1α, MIP-1α and IGF-2 were down-regulated, while 61 proteins were up-regulated. Bioinformatics analysis indicated that most DEPs were associated with leukocytes, among which IL-1α, SDF-1b, B7-1, CD40, CTLA4, IL-9, MIP-1α and CD40L were in the center of protein-protein interaction (PPI) network. Subsequently, the ability of these DEPs to distinguish GBS from healthy control was further evaluated. CD23 was identified by means of Random Forests Analysis (RFA) and verified by enzyme-linked immunosorbent assay (ELISA). The ROC curve result of CD23 respectively displayed that its sensitivity, specificity and AUC were 0.818, 0.800 and 0.824. We speculate that activation of leukocyte proliferation and migration in circulating blood might be associated with inflammatory recruitment of peripheral nerves, leading to the occurrence and development of GBS, but this conclusion still requires deeper confirmation. More importantly, central proteins may play a pivotal role in the pathogenesis of GBS. In addition, we detected IL-1α, IL-9, and CD23 in the serum of GBS patients for the first time, which may be promising biomarkers for the treatment of GBS.
格林-巴利综合征（GBS）是一种与感染和免疫机制有关的急性特发性多发性神经病。该病的确切发病机制尚不清楚，治疗也有限。因此，本研究旨在鉴定 GBS 血清中的生物标志物，并阐明其在 GBS 潜在发病机制中的作用，以帮助更准确地治疗 GBS。采用抗体芯片技术检测了 5 例 GBS 组和 5 例健康对照组血清中 440 种蛋白质的表达水平。抗体芯片鉴定出 67 个差异表达蛋白（DEPs），其中 FoLR1、Legumain、ErbB4、IL-1α、MIP-1α 和 IGF-2 下调，而 61 个蛋白上调。生物信息学分析表明，大多数 DEPs 与白细胞有关，其中 IL-1α、SDF-1b、B7-1、CD40、CTLA4、IL-9、MIP-1α 和 CD40L 处于蛋白-蛋白相互作用（PPI）网络的中心。随后，进一步评估了这些 DEPs 区分 GBS 与健康对照组的能力。通过随机森林分析（RFA）鉴定出 CD23，并通过酶联免疫吸附试验（ELISA）验证。CD23 的 ROC 曲线结果分别显示其灵敏度、特异性和 AUC 分别为 0.818、0.800 和 0.824。我们推测，循环血液中白细胞增殖和迁移的激活可能与周围神经的炎症募集有关，导致 GBS 的发生和发展，但这一结论仍需要更深入的证实。更重要的是，中枢蛋白可能在 GBS 的发病机制中起关键作用。此外，我们首次在 GBS 患者的血清中检测到了 IL-1α、IL-9 和 CD23，它们可能是治疗 GBS 的有前途的生物标志物。
