Elevated Levels of Cerebrospinal Fluid and Plasma Interleukin-37 in Patients with Guillain-Barré Syndrome

Cong Li,Pingwei Zhao,Yanfang Jiang,Yuanyuan Che,Xiguang Sun

doi:10.1155/2013/639712

Abstract

Aims. Interleukin-37 (IL-37) is an anti-inflammatory cytokine. This study aims to investigate the concentrations of plasma and cerebrospinal fluid (CSF) IL-37 in patients with Guillain-Barré Syndrome (GBS). Methods. The levels of plasma and CSF IL-37, IL-17A, IFN-γ, and TNF-α in 25 GBS patients and 20 healthy controls (HC) were determined by enzyme-linked immunoabsorbent assay and flow cytometric bead array assay, respectively. The values of clinical parameters in the patients were also measured. Results. The concentrations of plasma IL-37, IL-17A, IFN-γ, and TNF-α and CSF IL-37 and IL-17A in patients at the acute phase of GBS were significantly higher than those in the HC. The levels of plasma IL-37, IL-17A, IFN-γ, and TNF-α were positively correlated in those patients, and the levels of CSF IL-37 and IL-17A as well as the levels of plasma TNF-α were correlated positively with the GBS disability scale scores (GDSs) in those patients. Treatment with intravenous immunoglobulin significantly reduced the levels of plasma IL-37, IL-17A, IFN-γ, and TNF-α in the drug-responding patients. Conclusions. Our findings indicate higher levels of plasma and CSF IL-37 and IL-17A and other proinflammatory cytokines in patients with GBS.

Highlights

Guillain-Barresyndrome (GBS) is an autoimmune disease characterized by autoimmunity against the peripheral nerves, leading to an acute polyneuropathy [1]
To investigate the potential role of these cytokines, we examined the concentrations of plasma Interleukin cerebrospinal fluid (CSF) (IL)-37, IL-17A, IFN-γ, and TNF-α in 25 patients with new onset GBS and 20 healthy controls (HC) by Enzyme-Linked Immunosorbent Assay (ELISA) and cytometric bead array (CBA), respectively
We examined the concentrations of plasma and CSF IL-37, IL-17A, IFN-γ, and TNF-α in 25 patients with new onset GBS and 20 age- and gender-matched the HC

Summary

Introduction

Guillain-Barresyndrome (GBS) is an autoimmune disease characterized by autoimmunity against the peripheral nerves, leading to an acute polyneuropathy [1]. The main clinical features of GBS are progressive, symmetrical muscle weakness associated with depressed or absent deep tendon reflexes [3]. The weakness frequently involves respiratory muscles, rendering patients respirator-dependent [4]. Patients with GBS usually display albuminocytological dissociation in the cerebrospinal fluid (CSF) with abnormally increased levels of proteins but without increased numbers of cells during the first week of the acute phase of GBS [5]. During the pathogenic process of GBS, patients commonly show blood-nerve barrier (BNB) breakdown, cytokine leakage, and activated Tcell and macrophage infiltration in the peripheral nervous system (PNS) [6]. How proinflammatory and anti-inflammatory cytokines are associated with the development of GBS has not been clarified

Methods

Results

Conclusion