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Neuroprotective role of fibroblast growth factor‐2 in experimental autoimmune encephalomyelitis
Author(s) -
Rottlaender Andrea,
Villwock Hannah,
Addicks Klaus,
Kuerten Stefanie
Publication year - 2011
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2011.03450.x
Subject(s) - experimental autoimmune encephalomyelitis , myelin oligodendrocyte glycoprotein , remyelination , multiple sclerosis , myelin , neuroprotection , fibroblast growth factor , microglia , oligodendrocyte , immunology , central nervous system , basic fibroblast growth factor , biology , encephalomyelitis , inflammation , medicine , growth factor , neuroscience , receptor
Summary 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.