Clinical Significances Of Serum Interleukin-27 And Interleukin-35 Levels In Patients With Guillain-Barré Syndrome

ObjectiveGuillain-Barré syndrome(GBS) is an acute immune-mediated inflammatory polyneuropathy. In this study, we detected the levels of interleukin-27(IL-27) and interleukin-35(IL-35) in the serum of patients with GBS in their acute phase, and analyzed the relationships between them and the GBS subtypes, the severity and prognosis of the disease to determine their significances in the pathogenesis of GBS.MethodsA total of 50 patients with GBS and 35 sex- and age-matched healthy controls(HCs) were recruited from January 2014 to July 2015. 9 patients were classified with acute inflammatory demyelinating polyneuropathies(AIDP), 17 patients with acute motor axonal neuropathy(AMAN), 16 patients with acute motor-sensory axonal neuropathy(AMSAN), and 8 patients with Miller Fisher syndrome(MFS). The clinical data of all cases were collected, the GBS disability score(GDS) was assessed to evaluate the severity of the disease at 2 weeks after entry of the patients, and the Erasmus GBS outcome score(EGOS) was assessed to predict outcome of the patients. Using enzyme-linked immunosorbent assay(ELISA), the serum levels of IL-27 and IL-35 were detected in patients with GBS in their acute phase and HCs, the serum anti-GM1 and anti-GQ1 b antibodies were detected in patients with GBS. The expressions of serum IL-27 and IL-35 in acute phase of GBS and its different subtypes were analysed. The relationship between the levels of IL-27 or IL-35 and the clinical indicators were analysed.Results1. The average serum levels of IL-27 in acute phase of GBS and HCs were 182.02±109.57 pg/ml vs. 116.60±53.13 pg/ml. The average serum levels of IL-27 in acute phase of GBS were significantly higher than HCs(P=0.002). The average serum levels of IL-27 in acute phase of the axonal and demyelinating forms of GBS were 187.71±108.53 pg/ml vs. 211.46±120.35 pg/ml. The axonal and demyelinating forms of GBS expressed much higher levels of IL-27 than HCs(P=0.002, P=0.013, respectively), and there was no significant difference between the axonal and demyelinating forms of GBS(P=0.646). There was no significant correlation between serum IL-27 levels in acute phase of GBS and the GDS or the predicted fractions of patients(r=0.166, P=0.249; r=0.107, P=0.460). There was also no significant correlation between the serum IL-27 levels in acute phase of axonal and demyelinating forms of GBS and the GDS or the predicted fractions(r=0.090, P=0.571; r=0.015, P=0.926).2. The median serum levels of IL-35 in acute phase of GBS and HCs were 0.13(0, 0.83) ng/ml vs. 0.47(0.20, 2.58) ng/ml. The median serum levels of IL-35 in acute phase of GBS were significantly lower than HCs(P=0.029). The median serum levels of IL-35 in acute phase of the axonal and demyelinating forms of GBS were 0(0, 0.71)ng/ml vs. 0.85(0.13, 4.61) ng/ml. The axonal forms of GBS expressed much lower levels of IL-35 than the demyelinating forms of GBS or HCs(P=0.014, P=0.004, respectively), but there was no significant difference between demyelinating forms of GBS and HCs(P=0.562). There was a negative correlation between serum IL-35 levels in acute phase of the axonal forms of GBS and the GDS or the predicted fractions of the patients(r=-0.358, P=0.041; r=-0.416, P=0.016).Conclusions1. The serum levels of IL-27 were significantly elevated in acute phase of GBS disease. The axonal and demyelinating forms of GBS expressed much higher levels of IL-27 than HCs, and there was no significant difference between the axonal and demyelinating forms of GBS. There was no significant correlation between the serum IL-27 levels in acute phase of GBS or the subtypes and the GDS or the predictions for disability outcomes of the patients. These results suggest that IL-27 is involved in the pathogenesis of acute phase of GBS disease.2. The serum levels of IL-35 were significantly decreased in acute phase of GBS disease. The axonal forms of GBS expressed much lower levels of IL-35 than the demyelinating forms of GBS or HCs, but there was no significant difference between demyelinating forms of GBS and HCs. These results suggest that IL-35 maybe is involved in the pathogenesis of acute phase of axonal forms of GBS disease. There was a negative correlation between serum IL-35 levels in acute phase of the axonal forms of GBS and the GDS or the predictions for disability outcomes of the patients. These results suggest that IL-35 could be a clinical predictors of the severity and prognosis of the axonal forms of GBS disease.