Elevated osteopontin reflects systemic inflammation in experimental autoimmune encephalomyelitis.

Abstract

We examined the expression and localization of osteopontin (OPN) in various organs in mice with experimental autoimmune encephalomyelitis (EAE). To evaluate the level of OPN in blood and various tissues, enzyme-linked immunosorbent assay and western blot analysis of OPN were performed. The serum level of OPN was significantly increased in mice with EAE, and OPN was upregulated in all tissues examined, including the liver, kidneys, intestines, and spinal cord. OPN immunoreactivity was noted in inflammatory cells (mainly macrophages) and was enhanced in constitutively expressed cell types in the examined organs. In sum, OPN, a pro-inflammatory and immunomodulatory mediator, was elevated in all tissues following EAE induction, resulting in increased blood concentrations. These findings suggest that OPN may function as a key extracellular matrix component contributing to systemic disorders in autoimmune disease models.