IL-17 and IL-22 in Cerebrospinal Fluid and Plasma Are Elevated in Guillain-Barré Syndrome

Abstract

Guillain-Barré syndrome (GBS) is an acute autoimmune-mediated inflammatory demyelinating disease that causes rapidly progressing paralysis and occasionally respiratory failure. We hypothesized that interleukin (IL)-17 and IL-22 are elevated in GBS and participate in the autoimmune inflammatory response of GBS. We used sandwich enzyme-linked immunosorbent assay (ELISA) to measure the IL-17 and IL-22 levels in the CSF, and plasma from 22 GBS patients at the acute phase and 18 healthy controls (HC). The results show that CSF and plasma levels of IL-17 and IL-22 are elevated in GBS patients compared with HC. IL-17 and IL-22 levels in CSF, respectively, are correlated with GBS disability scale scores (GDSs). Meanwhile, IL-17 and IL-22 levels in CSF, IL-22 in CSF, and plasma of GBS patients have positive correlation, respectively. The increased levels of IL-17 and IL-22 in CSF may be explained by the disruption of blood-brain barrier (BBB) and peripheral nervous system (PNS) local inflammation in GBS. Meanwhile, the elevated levels of these two cytokines in plasma suggest the activation of Th17 and Th22 cells in the systemic immune response of GBS. Our data provide preliminary evidence that GBS is associated with high levels of IL-17 and IL-22 in CSF and plasma. These cytokines display pathogenic potential and may serve as useful biomarkers for GBS.

Expression of Early Growth Response Gene-2 and Regulated Cytokines Correlates with Recovery from Guillain–Barré Syndrome

“…The EGR2 or Krox-20 protein is a transcription factor involved in several processes such as immune response, early smooth musclelike cell differentiation, pathogenesis of fibrosis, and myelination in the peripheral nervous system with implications for the inherited peripheral neuropathies (5)(6)(7)(8)(9)(18)(19)(20). Furthermore, recent results have shown that EGR2 is induced by IL-6 and TGF-b and negatively regulates the expression of IL-17 but not IL-2 or IFN-g in effector T cells (20).…”

“…Furthermore, recent results have shown that EGR2 is induced by IL-6 and TGF-b and negatively regulates the expression of IL-17 but not IL-2 or IFN-g in effector T cells (20). The IL-6 and IL-17 are produced by activated Th17 cells, which are significantly increased in GBS patients (5)(6)(7)(8), and IL-17 and IL-22 levels have been implicated in the acute stage of GBS (7,8).…”

“…Although GBS is considered to be an autoimmune disease with the involvement of both cellular and humoral immune responses (2), little is known about the molecular mechanisms involved in the pathogenesis of GBS and its variants (2,(5)(6)(7)(8)(9). Strong evidence support a role for Th17 and IL-17 response in GBS (5)(6)(7)(8)(9), and that axonal subtypes of GBS, AMAN, and AMSAN are caused by Abs to gangliosides on the axolemma that target macrophages to invade the axon at the node of Ranvier (2).…”

“…Strong evidence support a role for Th17 and IL-17 response in GBS (5)(6)(7)(8)(9), and that axonal subtypes of GBS, AMAN, and AMSAN are caused by Abs to gangliosides on the axolemma that target macrophages to invade the axon at the node of Ranvier (2). About one-quarter of patients with GBS have suffered a recent bacterial or viral infection, and axonal forms of the disease are especially common in these patients (2,(10)(11)(12)(13)(14).…”

Differential gene expression of cytokines and neurotrophic factors in nerve and skin of patients with peripheral neuropathies

“…In two studies on CIDP, a major role of CD8-positive T cells was found, involving clonal cellular expansion in blood and nerve samples of these patients, linking systemic and local immune alterations [38,51]. Elevated interleukin-17 levels in different body fluids have also been described [19,[30][31][32].…”