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- W2556149069 abstract "OBJECTIVE: We investigated the effect of fingolimod in experimental autoimmune neuritis (EAN), a rat model of acute autoimmune peripheral polyneuritis (Guillain-Barre Syndrome).BACKGROUND: Fingolimod is an orally administered, active immunomodulator with neuroprotective potential approved for the treatment of relapsing-remitting multiple sclerosis. Its mechanisms of action in the peripheral nerves have not been examined systematically yet however there are some reports regarding an influence on Schwann cells survival in vitro.METHODS: Active EAN was induced by immunization with the P2 aa 53-78 myelin peptide in Lewis rats followed by oral treatment with 1 to 3mg/kg Fingolimod diluted in rapeseed oil once daily from day 1 to 23 post-immunisation (p.i.), and clinical score was assessed daily. Electrophysiological analysis of demyelination as well as histological analyses of the sciatic nerves regarding demyelination, early axonal damage (amyloid precursor protein, APP), inflammatory infiltrates, Schwann cells survival (TUNEL) and ICAM1 (intracellular adhesion molecule 1) expression were performed at the disease maximum (day 16 p.i.).RESULTS: Preventive treatment with oral Fingolimod diluted in rapseed oil at all concentrations tested completely abolished clinical neuritis by reducing signs of demyelination in the nerve conduction studies. Histological analyses revealed a significantly lower degree of T cells and macrophages infiltrates in the sciatic nerves. In addition, we detected a reduction of early signs of axonal degeneration through a reduction of APP expressed in axons of the peripheral nerves. This reduction correlated with an increase of Schwann cells survival and a reduction of ICAM-1 expression at the disease maximum indicating the effects of fingolimod on blood-nerve barrier permeability during inflammation.CONCLUSIONS: The effect on blood-nerve barrier permeability and on Schwann cell survival in vivo represent new mechanisms of action of Fingolimod in peripheral neuritis and imply a crucial neuroprotective potential of this substance. Disclosure: Dr. Ambrosius has nothing to disclose. Dr. Pitarokoili has nothing to disclose. Dr. Schrewe has nothing to disclose. Dr. Gold has received research support from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis, and Teva Neuroscience." @default.
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- W2556149069 date "2016-04-05" @default.
- W2556149069 modified "2023-09-23" @default.
- W2556149069 title "Antiiflammatory and Neuroprotective Role of Fingolimod in Experimental Autoimmune Neuritis in Lewis Rats (S28.007)" @default.
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