Abstract
IL-23 and IL-27 are believed to be involved in the pathogenesis of Guillain-Barré syndrome (GBS). However, changes in these cytokines during the dynamic pathological and recovery processes of GBS are not well described. In the present study, plasma was collected from 83 patients with various stages of GBS, 70 patients with central nervous system demyelinating diseases,70 patients with other neurological diseases (OND) and 70 age- and sex-matched healthy volunteers. Serum levels of IL-23, IL-27, and Campylobacter jejuni (CJ) IgM were assessed using enzyme linked immunosorbent assay (ELISA). We found that serum IL-23 levels of patients during the acute phase of GBS were significantly higher followed by a decreasing trend during the recovery phase of the disease. Serum IL-27 levels significantly increased during the acute phase of GBS, and gradually increased during the recovery phase. Interestingly, both the severity and subtype of GBS were closely associated with the two cytokines. IL-23 levels were positively correlated with IL-27 levels, prognosis, and other clinical parameters. Our findings confirm that IL-23 may show pro-inflammatory effects, especially at the early stage of GBS. IL-27 appears to have a dual role in GBS, with initial pro-inflammatory effects, followed by anti-inflammatory properties during recovery.
Highlights
Guillain-Barré syndrome (GBS) is an autoimmune-mediated neurological disorder affecting peripheral nerves
Recent research demonstrated that IL-27 levels are increased in the cerebral spinal fluid (CSF), but not the sera, of relapsing remitting multiple sclerosis (RRMS) patients compared to healthy donors, and that IL-27 is expressed by astrocytes in active MS plaques[19]
We found that the IL-23 levels in the serum of GBS patients distinctly increased during the acute phase of GBS compared to other groups, and decreased during the recovery phase at 1, 3 and 6 months following disease onset
Summary
Guillain-Barré syndrome (GBS) is an autoimmune-mediated neurological disorder affecting peripheral nerves It is characterised by weakness of limbs and areflexia, and progresses for up to four weeks[1]. Recent research demonstrated that IL-27 levels are increased in the cerebral spinal fluid (CSF), but not the sera, of relapsing remitting multiple sclerosis (RRMS) patients compared to healthy donors, and that IL-27 is expressed by astrocytes in active MS plaques[19]. Together, this supports the hypothesis that IL-27 may suppress the effector phase of immune-mediated disorders. Another recent study found that IL-27 might be pathogenic in GBS20
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