Intravenous immunoglobulin preparations attenuate lysolecithin-induced peripheral demyelination in mice and comprise anti-large myelin protein zero antibody

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  • SETOGUCHI Yuki
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • HAYASHI Akiko
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • KAWADA Ayami
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • IBUSUKI Ayako
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • YANAOKA Daigo
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • SAITO Ryota
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • ISHIBASHI Tomoko
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • TAKIMOTO Hiroaki
    Department of Biosciences, School of Science, Kitasato University
  • YAMAGUCHI Yoshihide
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • OHTAKI Hirokazu
    Department of Functional Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
  • BABA Hiroko
    Department of Occupational Therapy, Faculty of Rehabilitation, Niigata University of Health and Welfare

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<p>Intravenous immunoglobulin (IVIg) has been used to treat inflammatory demyelinating diseases such as chronic inflammatory demyelinating polyneuropathy, Guillain–Barré syndrome, and multifocal motor neuropathy. Despite studies demonstrating the clinical effectiveness of IVIg, the mechanisms underlying its effects remain to be elucidated in detail. Herein, we examined the effects of IVIg on lysolecithin-induced demyelination of the sciatic nerve in a mouse model. Mice —administered with IVIg 1 and 3 days post-injection (dpi) of lysolecithin —exhibited a significantly decreased demyelination area at 7 dpi. Immunoblotting analysis using two different preparations revealed that IVIg reacted with a 36-kDa membrane glycoprotein in the sciatic nerve. Subsequent analyses of peptide absorption identified the protein as a myelin protein in the peripheral nervous system (PNS) known as large myelin protein zero (L-MPZ). Moreover, injected IVIg penetrated the demyelinating lesion, leading to deposition on L-MPZ in the myelin debris. These results indicate that IVIg may modulate PNS demyelination, possibly by binding to L-MPZ on myelin debris.</p>

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