title: Reduced soluble RAGE is associated with disease severity of axonal Guillain-Barré syndrome.
abstract: Soluble receptor for advanced glycation end products (sRAGE) is an anti-inflammatory factor that mitigates the proinflammatory effects of high mobility group box 1 (HMGB1). The aim of this study was to investigate whether Guillain-Barré syndrome (GBS)-related inflammation are mediated by sRAGE and HMGB1. We measured serum sRAGE, HMGB1, IL-6, and TNF-α levels in 86 patients with GBS and analysed associations between sRAGE or HMGB1 and clinical variables in these subjects. In addition, we determined cerebrospinal fluid sRAGE and HMGB1 levels in a cross-sectional study of 50 patients with GBS who had matched serum samples. We found serum sRAGE levels in patients with the acute motor axonal neuropathy (AMAN) subtype of GBS, but not other subtypes, were significantly lower than those in healthy controls, and were significantly correlated with GBS disability score and Erasmus GBS outcome score, while serum HMGB1, IL-6, and TNF-α levels in all subtypes of GBS were significantly higher than those in healthy controls. Moreover, increased sRAGE levels and decreased HMGB1 levels after treatment were observed. Our results showed that serum sRAGE may be a useful biomarker for inflammation in the AMAN GBS subtype, while HMGB1 may be related to the inflammatory process across all types of GBS.
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Da-Qi
authors.initials: DQ
authors.lastname: Zhang
authors.affiliation: School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
authors.forename: Rong
authors.initials: R
authors.lastname: Wang
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Li
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Jian-Ping
authors.initials: JP
authors.lastname: Zhou
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Guo-Qiang
authors.initials: GQ
authors.lastname: Chang
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Zhao
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Yang
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Zhai
authors.affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Li
authors.initials: L
authors.lastname: Yang