![]() This study analyzed relationships between RSNO, and IL-6 CSF level as well as pNfh levels with the aim of accurately evaluating the severity of axonal damage at the moment of sampling and erythropoietin (EPO) levels as a marker of anti-inflammatory defense in patients with demyelinating disorders. 14 It therefore seemed reasonable to explore potential associations between RSNO and IL-6 levels in MS and other demyelinating disorders (NMOSD and ADEM) while controlling for neurodegeneration processes using CSF levels of phosphorylated neurofilament heavy chain (pNfh). We previously demonstrated an association between the serum S-nitrosothiols (RSNO) level and spinal-cord injury. 13 suggested that different nitric oxide (NO) expression levels in the brain and spinal cord are associated with specific IL-6 pathways. 12 Thus, how IL-6R blockade influences the progression of demyelination in different demyelinating disorders remains obscure.Ĭurrent challenges in the management of patients with demyelinating disorders are related to the lack of biomarkers useful for stratifying their different clinical forms. 11 These different responses to IL-6R blockade may be due to different patterns of B-cell activation and prominent IL-6 involvement in NMOSD, which has not been identified in MS so far. IL-6R blockade with the monoclonal antibody tocilizumab has successfully used in NMOSD, 9 though other case reports demonstrated MS arising during tocilizumab therapy in rheumatoid arthritis patients 10 and MS-like demyelinating disorders were described due to tocilizumab treatment. The CSF IL-6 levels in these patients were correlated with the length of the spinal-cord lesion and anti-AQP4-antibody positivity, and they decreased after treatment. 8 reported that a CSF IL-6 cut-off of 7.8 pg/mL produced a sensitivity of 73.17% and a specificity of 76.94%, which can provide a strong additional diagnostic marker for NMOSD among other patients with neurological disorders. 7 found that a CSF IL-6 cut-off of 10 pg/mL provided a sensitivity of 96% for excluding MS, and in such cases other inflammatory disorders should be suggested. However, IL-6 levels were found to be higher in NMOSD patients than in both MS patients and controls 4 notably, a higher IL-6 level in the peripheral blood in NMO was associated with the production of anti-aquaporin-4 (AQP4) antibodies, 5 which could result from the increased survival of plasmablasts producing AQP4 antibodies. ![]() 3 reported that IL-6 levels in cerebrospinal fluid (CSF) were higher in MS patients than in controls. In demyelinating lesions, IL-6 is secreted by infiltrating leukocytes, local microglia, and activated astrocytes. IL-6 can be produced by a wide variety of cells, including macrophages, mast cells, dendritic cells, activated T- and B-cells as well as several types of nonhematopoietic cells, including astrocytes and fibroblasts. IL-6 exerts its cellular effects via two distinct pathways: the first pathway involves the membrane-bound interleukin-6 receptor (IL-6R) that is expressed on microglia and other cells and acts via the β-receptor glycoprotein 130, while the alternative pathway is trans-signaling via a soluble form of the IL-6R capable of binding IL-6. IL-6 is crucial for the activation of immune cells and can act as a neurotrophic factor. Interleukin-6 (IL-6) is recognized as an important cytokine involved in inflammatory diseases of the central nervous system (CNS). ![]() ![]() 1 However, the activation profile of cytokines varies with the demyelination pattern. The data reported by a few groups suggest that activated cytokines and nitrosative stress are closely involved in the pathophysiology of different demyelinating disorders via the induction of the neuroinflammatory destruction of neurons. Acquired demyelinating syndromes in adults include multiphasic diseases such as multiple sclerosis (MS), neuromyelitis optica (NMO), and neuromyelitis optica spectrum disorders (NMOSD), and monophasic diseases such as acute disseminated encephalomyelitis (ADEM). ![]()
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