Диагностический и терапевтический потенциал resolvin D1 в синдроме Гильен-Барре.
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Wang Ying, Liu Shan, Zhu Mingqin, Zhang Qingxiang, Sun Hui, Liu Kangding, Zhu Jie
Аннотация
Оригинал публикации
Diagnostic and therapeutic potential of resolvin D1 in Guillain-Barré syndrome.
INTRODUCTION: Most neuroimmune diseases are incurable and require lifelong immunotherapy, whereas Guillain-Barré syndrome (GBS), a peripheral nervous system autoimmune disorder, has a relatively favorable prognosis. Investigating the molecular disparities underlying recovery between GBS and other neuroimmune diseases may facilitate the development of innovative therapeutic strategies.
OBJECTIVES: This study explored the diagnostic and therapeutic potential of resolvin D1 (RvD1), a specialized pro-resolving mediator that promotes inflammation resolution and tissue regeneration, in GBS and its animal model experimental autoimmune neuritis (EAN).
METHODS: Serum RvD1 levels were measured in 218 participants from two cohorts, including healthy controls (HCs), GBS patients, and those with multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), or stroke. The diagnostic accuracy was evaluated via the area under the receiver operating characteristic (ROC) curve (AUC). RvD1 was administered to EAN and experimental autoimmune encephalomyelitis (EAE, an MS animal model) to assess its therapeutic efficacy.
RESULTS: Serum RvD1 was elevated in GBS patients, demonstrating high diagnostic accuracy in differentiating GBS patients from HCs (cohort 1: AUC 0.72; cohort 2: AUC 0.93), MS/NMOSD patients (cohort 1: AUC 0.83), and stroke patients (cohort 1: AUC 0.68). The RvD1 level continued to increase as GBS progressed and was positively correlated with disease severity, ventilator dependence, and axonal neuropathy. In EAN, RvD1 and its synthetase/receptor were upregulated in serum, spleen, and sciatic nerve, exhibiting tissue-specific inflammation resolution patterns across disease phases. RvD1 treatment promoted inflammation resolution in EAN, as evidenced by attenuated disease severity and autoimmune responses, with its therapeutic effect was translatable to EAE.
CONCLUSION: RvD1 may serve as a biomarker for both diagnosing GBS and monitoring disease severity. It represents a potential immunotherapeutic agent for GBS and other neuroimmune disorders. Elucidating the molecules associated with recovery in patients with GBS may facilitate the discovery of novel therapeutic strategies for neuroimmune disorders.