Créange A, Bélec L, Clair B, Degos J D, Raphaël J C, Gherardi R K
Réseau de Neuroimmunologie du Nerf Périphérique (AP/HP), Créteil, France.
J Neurol Neurosurg Psychiatry. 1998 Feb;64(2):162-5. doi: 10.1136/jnnp.64.2.162.
To delineate the possible implication of the immunosuppressive cytokine transforming growth factor beta 1 (TGF-beta1) in the pathogenesis of Guillain-Barré syndrome. Guillain-Barré syndrome is a disorder that may implicate cytokines in its pathogenesis. TGF-beta1 is a potent anti-inflammatory cytokine occasionally shown to be regulated in the course of demyelinating disorders.
The study measured circulating proinflammatory and anti-inflammatory cytokines from the progressing phase to early recovery in patients with Guillain-Barré syndrome. Plasma concentrations of TNF-alpha, IL-beta1, IL-2, IL-4, IL-6, IL-10, and TGF-beta1 were prospectively evaluated in 15 patients with Guillain-Barré syndrome every three days for the first 15 days after admission to hospital, and in 15 controls with non-inflammatory neurological diseases.
Concentrations of TGF-beta1 in plasma were decreased in 13115 patients (87 %) at day 1, remained low during progression and the plateau of paralysis (days 1-10), and then progressively increased up to control concentrations during early recovery (days 12-15). Concentrations of plasma TGF-beta1 correlated positively with motor function, the lowest values being e found in the most disabled patients. Concentrations of plasma TGF-beta1 were decreased before any treatment, and during treatment by either plasma exchange or intravenous immunoglobulins, plasma exchange being associated with a more pronounced decrease in TGF-beta1 at day 7. Circulating TNF-alpha concentrations were raised, as previously reported, when other cytokines were either randomly increased (IL-2, IL-6), or undetectable (IL-1, IL-4, IL-7, IL-10).
Down regulation of TGF-beta1 in the early course of Guillain-Barré syndrome could participate in neural inflammation.
探讨免疫抑制细胞因子转化生长因子β1（TGF-β1）在吉兰-巴雷综合征发病机制中的可能作用。吉兰-巴雷综合征是一种发病机制可能与细胞因子有关的疾病。TGF-β1是一种强效抗炎细胞因子，在脱髓鞘疾病过程中偶尔会出现其调节异常。
本研究检测了吉兰-巴雷综合征患者从病情进展期到早期恢复阶段循环中的促炎和抗炎细胞因子。对15例吉兰-巴雷综合征患者入院后的前15天每3天进行一次血浆肿瘤坏死因子-α（TNF-α）、白细胞介素-β1（IL-β1）、白细胞介素-2（IL-2）、白细胞介素-4（IL-4）、白细胞介素-6（IL-6）、白细胞介素-10（IL-10）和TGF-β1浓度的前瞻性评估，并与15例非炎性神经系统疾病对照者进行比较。
15例患者中有13例（87%）在第1天时血浆TGF-β1浓度降低，在病情进展和瘫痪高峰期（第1 - 10天）持续保持低水平，然后在早期恢复阶段（第12 - 15天）逐渐升高至对照浓度。血浆TGF-β1浓度与运动功能呈正相关，功能最差的患者血浆TGF-β1浓度最低。在任何治疗前以及血浆置换或静脉注射免疫球蛋白治疗期间，血浆TGF-β1浓度均降低，血浆置换在第7天时与TGF-β1更明显的降低相关。如先前报道，当其他细胞因子随机升高（IL-2、IL-6）或无法检测到（IL-1、IL-4、IL-7、IL-10）时，循环TNF-α浓度升高。
吉兰-巴雷综合征病程早期TGF-β1的下调可能参与神经炎症反应。
