Abstract
Guillain–Barré syndrome (GBS) is an acute fatal progressive disease caused by autoimmune mechanism mainly affecting peripheral nervous system. Although the syndrome is clinically sub-classified into several variants, specific biomarker and exact pathomechanism of each subtypes are not well elucidated yet. In current study, integrative metabolomic and lipidomic profiles were acquisitioned from cerebrospinal fluid samples of 86 GBS from three variants and 20 disease controls. And the data were systematically compared to our previous result on inflammatory demyelination disorders of central nervous system (IDDs) and healthy controls. Primary metabolite profiles revealed unique metabolic traits in which 9 and 7 compounds were specifically changed in GBS and IDD, respectively. Next, the biomarker panel with 10 primary metabolites showed a fairly good discrimination power among 3 GBS subtypes, healthy controls, and disease controls (AUCs ranged 0.849–0.999). The robustness of the biomarker panel was vigorously validated by multi-step statistical evaluation. Subsequent lipidomics revealed GBS variant-specific alteration where the significant elevations of lyso-phosphatidylcholines and sphingomyelins were unique to AIDP (acute inflammatory demyelinating polyneuropathy) and AMAN (acute motor axonal neuropathy), respectively. And metabolome-wide multivariate correlation analysis identified potential clinical association between GBS disability scale (Hughes score) and CSF lipids (monoacylglycerols, and sphingomyelins). Finally, Bayesian network analysis of covarianced structures of primary metabolites and lipids proposed metabolic hub and potential biochemical linkage associated with the pathology.
Highlights
Guillain-Barre syndrome (GBS) is an acute inflammatory peripheral neuropathy
Subsequent lipidomics revealed Guillain–Barré syndrome (GBS) variant-specific alteration where the significant elevations of lyso-phosphatidylcholines and sphingomyelins were unique to acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN), respectively
Comparative analysis following batch effect removal process was conducted against healthy controls and inflammatory demyelination disorders of central nervous system (IDDs) obtained from our recent study[12,14] in order to delineate disorders of peripheral nervous system from central nervous system
Summary
Guillain-Barre syndrome (GBS) is an acute inflammatory peripheral neuropathy. It is rare, but once it develops, a portion of patients is accompanied by a serious clinical course. Several types of GBS have been identified and recent studies have revealed that some of these subtypes were determined by specific anti-ganglioside antibodies[2]. It included acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and Miller Fisher syndrome (MFS) according to clinical, electrophysiological, and immunological information[3,4,5]. Our study aimed to investigate unique metabolic profiles of three GBS variants (AIDP, AMAN, and MFS) by applying multiplex instrumental analysis on CSF samples. Comparative analysis following batch effect removal process was conducted against healthy controls and IDDs (multiple sclerosis and neuromyelitis optica spectrum disorder) obtained from our recent study[12,14] in order to delineate disorders of peripheral nervous system from central nervous system
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