摘要：Abstract Background Neuromyelitis optica (NMO) is an inflammatory disease of the central nervous system that predominantly affects the optic nerves and spinal cord. Although {NMO} has long been considered a subtype of multiple sclerosis (MS), the effects of interferon-β treatment are different between {NMO} and MS. Recent findings of NMO-IgG suggest that {NMO} could be a distinct disease rather than a subtype of MS. However, the underlying molecular mechanism of {NMO} pathology remains poorly understood. Methods {OPN} in the cerebrospinal fluid and brain of patients with {NMO} and with MS, as well as of patients with other neurologic disease/idiopathic other neurologic disease was examined using Western blotting, ELISA, immunohistochemistry and Boyden chamber. Results Here we show that osteopontin is significantly increased in the cerebrospinal fluid of {NMO} patients compared with {MS} patients. Immunohistochemical analyses revealed that osteopontin was markedly elevated in the cerebral white matter of {NMO} patients and produced by astrocytes, neurons, and oligodendroglia as well as infiltrating macrophages. We also demonstrate that the interaction of the cerebrospinal fluid osteopontin in {NMO} patients with integrin αvβ3 promoted macrophage chemotaxis by activating phosphoinositide 3-kinase and MEK1/2 signaling pathways. Conclusion These results indicate that osteopontin is involved in {NMO} pathology. General significance Thus therapeutic strategies that target osteopontin signaling may be useful to treat NMO.
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