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Microglial/macrophage activation in the cerebrospinal fluid of neuromyelitis optica spectrum disorders

AIM: The aims of this pilot study were to investigate the levels of biomarkers of microglial/macrophage activation—YKL‐40, sCD163, and sCD14—in patients with neuromyelitis optica spectrum disorder (NMOSD) and determine the possible associations between these biomarkers and Expanded Disability Status...

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Detalles Bibliográficos
Autores principales: Li, Jinghong, He, Yan, Wang, Honghao, Chen, Jinyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9759122/
https://www.ncbi.nlm.nih.gov/pubmed/36306394
http://dx.doi.org/10.1002/brb3.2798
Descripción
Sumario:AIM: The aims of this pilot study were to investigate the levels of biomarkers of microglial/macrophage activation—YKL‐40, sCD163, and sCD14—in patients with neuromyelitis optica spectrum disorder (NMOSD) and determine the possible associations between these biomarkers and Expanded Disability Status Scale (EDSS) scores. METHODS: We measured the levels of three microglia‐/macrophage‐related proteins (YKL‐40, soluble CD163, and soluble CD14) in cerebrospinal fluid (CSF) using enzyme‐linked immunosorbent assays. In addition, patients’ neurological disability levels were assessed using EDSS scores. RESULTS: NMOSD patients had significantly higher CSF levels of YKL‐40(210.52 ± 161.62 for NMOSD and 63.18 ± 9.22 for control), sCD163 (87.23 ± 56.85 for NMOSD and 58.14 ± 7.66 for control), and sCD14 (68.22 ± 24.11 for NMOSD and 55.75 ± 9.48 for control) compared with controls. Furthermore, these biomarker levels were positively correlated with EDSS scores in patients with NMOSD (r = 0.303, p = .002 for YKL‐40; r = 0310, p = .001 for sCD14; r = 0.250, p = .011 for sCD163), but not in patients with multiple sclerosis or glial fibrillary acidic protein astrocytopathy. CONCLUSION: Our findings suggest that microglial/macrophage activation may be implicated in the pathogenesis of NMOSD.