Neuroprotective role of fibroblast growth factor‐2 in experimental autoimmune encephalomyelitis

Abstract

The role of fibroblast growth factor-2 (FGF-2) in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis is discussed. This study is the first to use FGF-2(-/-) mice to further address the involvement of FGF-2 in the disease process. We demonstrate that immunization with myelin oligodendrocyte glycoprotein peptide 35-55 induces more severe experimental autoimmune encephalomyelitis in FGF-2(-/-) mice compared with FGF-2(+/+) mice. The antigen-specific cytokine response to myelin oligodendrocyte glycoprotein peptide and the degree of central nervous system inflammation was similar in both groups. However, FGF-2(-/-) mice displayed increased infiltration of CD8(+) T cells and macrophages/microglia. In addition, nerve fibre degeneration and axonal loss were augmented, whereas the extent of remyelination in central nervous system lesions was reduced. FGF-2 has been associated with the induction of demyelination and the inhibition of myelin production by oligodendrocytes. Our study supports the opposing notion that FGF-2 can also assert a neuroprotective function. This may be particularly appealing when it comes to targeting the neurodegenerative aspect of multiple sclerosis.