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.
Bibliographical noteFunding Information:
This work was financially supported by the National Research Foundation of Korea (NRF) Grant (NRF-2014M3A9B6069340, NRF-2016R1C1B2007982, NRF-2018M3A9F3020970, and NRF-2016R1D1A1B03931783) funded by the Korean Ministry of Science, ICT and Future Planning. This study was also supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (2016R1A5A2007009). We thank Young-Eun Park, Eun Hee Sohn, Min Su Park, and Dae-Seong Kim for collecting clinical and demographic data and performing preliminary statistics.
© 2019, The Author(s).
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