Significance Of Of Soluble RAGE And HMGB1 Detection In Patients With Guillain-Barré Syndrome

Objectives Guillain-Barré Syndrome(GBS)is a clinically heterogeneous autoimmune-mediated polyneuropathy of the peripheral nervous system.GBS clinical subtypes,such as acute inflammatory demyelinating polyneuropathy(AIDP)and acute motor axonal neuropathy(AMAN),have different epidemiological and clinical characteristics.This suggests that there may be distinctive pathogenic mechanisms underlying each subtype of GBS.Recent studies have shown that the soluble receptor for advanced glycation end products(s RAGE)and the high mobility group box 1(HMGB1)-advanced glycation end products are anchored to the plasma membrane.The signaling pathway of the membrane-bound receptor for advanced glycation end products(m RAGE)plays an important role in the development of many autoimmune diseases.The aim of this study was to determine whether s RAGE and HMGB1-m RAGE signaling pathways are involved in the development of GBS,and to explore their role in the various subtypes of GBS in order to identify potential biological markers of disease severity.Methods Serum and/or cerebrospinal fluid(CSF)specimens were collected from 86 fully compliant GBS patients with detailed clinical information,as well as 25 patients with non-inflammatory neurological diseases,and 60 healthy volunteers.The levels of s RAGE,HMGB1,tumor necrosis factor-?(TNF-?),and interleukin-6(IL-6)in serum and cerebrospinal fluid were measured using the enzyme-linked immunosorbent assay to analyze the relationship between the HMGB1-m RAGE signaling pathway,disease subtypes,and disease severity,and also their respective levels before and after treatment.Results 1.Serum s RAGE levels in patients with GBS and its subtype AMAN were significantly lower than those in healthy controls(P<0.001).In patients with AMAN,serum s RAGE levels were significantly negatively correlated with GBS disability status scores(r=-0.445,P<0.001).2.The levels of serum HMGB1,IL-6,and TNF-? in GBS and its subtypes were significantly higher than those in healthy controls(P<0.001;P=0.033;P=0.026).However,the serum levels and GBS disability scores were not significantly correlated(P>0.05).3.Compared with pre-treatment,serum s RAGE levels in patients with GBS during treatment and after treatment reached a plateau were significantly increased(P<0.001;P=0.004),while HMGB1 levels were significantly decreased(P=0.033;P=0.014).4.Serum s RAGE levels were significantly negatively correlated with the Erasmus GBS outcome score(EGOS)in patients with AMAN when compared with healthy controls(r =-0.340,P < 0.014),whereas serum HMGB1 levels were not significantly associated with the EGOS(r =-0.340,P<0.014).5.GBS patients with decreased serum s RAGE levels and elevated HMGB1 had a significantly higher GBS disability score and EGOS than other GBS patients(p=0.006;p=0.002).6.The levels of s RAGE and HMGB1 in cerebrospinal fluid of GBS patients were not statistically different from those in the control group(P>0.05).Conclusion 1.Serum s RAGE levels were significantly decreased in GBS patients,while the levels of HMGB1,IL-6,and TNF-? were significantly increased,suggesting that s RAGE and HMGB1-m RAGE signaling pathways may be involved in the development of GBS.2.Serum s RAGE levels were significantly reduced in patients with the GBS subtype AMAN and were significantly negatively correlated with GBS disability status scores and EGOS,suggesting that serum s RAGE may be a biological marker for detecting the severity of AMAN.