Abstract
Background: Guillain Barré Syndrome (GBS) is an autoimmune disorder caused by the immune-mediated damage of the peripheral nervous system. Increasing evidence suggests that inflammatory cytokines are important mediators for the onset and progression of GBS. A number of clinical studies have demonstrated elevated levels of T helper-1 (Th1-), Th2-, and Th17-related cytokines in patients with GBS; however, the results were inconsistent across studies.Methods: We performed a systematic review and a meta-analysis of studies comparing the levels of inflammatory cytokines in the cerebrospinal fluid and peripheral blood between patients with GBS and healthy individuals, using Comprehensive Meta-Analysis Version 2 software. A database search identified 30 studies comprising 1,302 patients with GBS and 1,073 healthy controls.Results: The random-effects meta-analysis demonstrated that peripheral blood tumor necrosis factor-α (Hedges g, 1.544; 95% confidence interval (CI), 0.923–2.165; p < 0.001), interleukin-1β (IL-1β; Hedges g, 0.678; 95% CI, 0.183–1.172; p = 0.007), IL-6 (Hedges g, 0.630; 95% CI, 0.100–1.160; p = 0.02), IL-4 (Hedges g, 0.822; 95% CI, 0.220–1.423; p = 0.007), IL-17 (Hedges g, 1.452; 95% CI, 0.331–2.573; p = 0.011), interferon-γ (Hedges g, 1.104; 95% CI, 0.490–1.719; p < 0.001), and C-reactive protein (Hedges g, 0.909; 95% CI, 0.453–1.365; p < 0.001) levels were significantly increased in patients with GBS when compared with healthy controls. Contrastingly, the blood IL-10 and transforming growth factor-β levels were not significantly associated with GBS. Furthermore, the meta-analysis found that cerebrospinal fluid IL-17 levels were significantly associated with GBS (Hedges g, 1.882; 95% CI, 0.104–3.661; p = 0.038).Conclusion: Altogether, our results clarified the circulating inflammatory cytokine profile in patients with GBS, and revealed that Th1-, Th2-, and Th17-related cytokines were highly elevated in the GBS patients, suggesting the potential use of these cytokines as biomarkers for GBS.
Highlights
Guillain Barré Syndrome (GBS) is an immune-mediated disorder of the peripheral nervous system characterized by muscle weakness (Eldar and Chapman, 2014)
Several studies demonstrated that the levels of inflammatory cytokines–tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interferon-γ (IFN-γ), and IL-17–were elevated in the patients with GBS compared to healthy controls (Hohnoki et al, 1998; Ossege et al, 2000; Nyati et al, 2011; Han et al, 2014)
Random-effects meta-analysis showed that patients with GBS had significantly elevated TNF-α (Hedges g, 1.544; 95% confidence interval (CI), 0.923–2.165; p < 0.001), IL-1β (IL-1β; Hedges g, 0.678; 95% CI, 0.183–1.172; p = 0.007), IL-6 (Hedges g, 0.630; 95% CI, 0.100–1.160; p = 0.02), IL-4 (Hedges g, 0.822; 95% CI, 0.220–1.423; p = 0.007), IL-17 (Hedges g, 1.452; 95% CI, 0.331–2.572; p = 0.011), IFN-γ (Hedges g, 1.104; 95% CI, 0.490– 1.719; p < 0.001), and C-reactive protein (CRP; Hedges g, 0.909; 95% CI, 0.453–1.365; p < 0.001) levels when compared with healthy controls (Figures 2, 3; Table 1)
Summary
Guillain Barré Syndrome (GBS) is an immune-mediated disorder of the peripheral nervous system characterized by muscle weakness (Eldar and Chapman, 2014). It has been proposed that a series of immune responses including macrophage and complement activation, and T-cell mediated cytotoxicity causes the demyelination of the peripheral nervous system and axonal damage leading to the onset of GBS (Hartung and Toyka, 1990; Wanschitz et al, 2003; Debnath et al, 2018b). It is well-known that the integrated actions of various cytokines play crucial roles in the differentiation and activation of immune cells such as B lymphocytes, T lymphocytes, and macrophages. A number of clinical studies have demonstrated elevated levels of T helper-1 (Th1-), Th2-, and Th17-related cytokines in patients with GBS; the results were inconsistent across studies
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