ArticleFrontiers in neurology
Dyslipidemia is associated with monocyte lipid metabolic reprogramming in Guillain-Barré syndrome.
Article in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
GBS (Guillain-Barré syndrome) is an acute immune-mediated peripheral neuropathy whose pathological mechanisms remain incompletely understood. Our study aimed to explore the intrinsic link and potential mechanisms between circulating dyslipidemia and immune metabolic remodeling of monocytes in GBS. Clinical data from 163 patients diagnosed with classic GBS and 169 healthy controls were analyzed to examine the correlations between their lipid profiles and immune cell features. Leveraging our team's previously published single-cell RNA sequencing (scRNA-seq) dataset for GBS, we characterized the subpopulations, functional features, and differentiation trajectories of peripheral blood monocytes. Furthermore, through transcriptional regulatory network analysis, we identified key transcription factors governing these processes. Compared to healthy controls, GBS patients displayed a distinct dyslipidemia characterized by elevated triglycerides (TG), very low-density lipoprotein (VLDL), and residual cholesterol (RC), but decreased high-density lipoprotein (HDL) and apolipoprotein A1 (APOA1). This lipid profile coincided with higher monocyte counts in peripheral blood, suggesting a synergistic relationship. The scRNA-seq analysis results indicate that the composition of peripheral blood monocyte subsets in GBS patients undergoes fundamental remodeling. This is characterized by a significant expansion of CD14
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