Experimental Allergic Neuritis Induced by Sensitization with Galactocerebroside

Abstract

Thirteen of 31 rabbits immunized repeatedly with bovine brain galactocerebroside developed experimental allergic neuritis, manifested by flaccid paresis and hypesthesia of four limbs, 2 to 11 months after the initial inoculation. Electrophysiological studies revealed multifocal conduction block of peripheral nerves. Perivenular demyelinative lesions associated with phagocytic mononuclear cells occurred in spinal ganglia, roots, and less frequently in distal nerves.

Molecular mimicry: Sensitization of Lewis rats with Campylobacter jejuni lipopolysaccharides induces formation of antibody toward GD3 ganglioside

“…Animal models of axonal injury with Wallerian-like degeneration in the peripheral nervous system have been reported to be induced in rabbits (sensitization with GM1, BBG, or LPS) and rats (sensitization with SGPG; Saida et al, 1979;Maeda et al, 1991;Yamawaki et al, 1996;Yuki et al, 2001Yuki et al, , 2004. Kusunoki et al (1996) also reported a model for experimental sensory neuropathy induced by sensitization of rabbits using purified GD1b.…”

“…To validate this mechanism, many attempts have been made to establish animal models of GBS by sensitizing laboratory animals (e.g., rabbit, rat, chicken, or mouse) with a variety of GSLs, such as sulfated glucuronosyl paragloboside (SGPG), GM1, bovine brain ganglioside mixture (BBG), or LPS (Yuki et al, 2004;Ariga and Yu, 2005). We have previously established rat and rabbit models of demyelinating paraproteinemia by sensitization of these animals with SGPG that revealed minor but clear clinical signs of neuropathy, including muscle weakness and conduction blocks in sciatic nerve (Kohriyama et al, 1988;Yamawaki et al, 1996).Animal models of axonal injury with Wallerian-like degeneration in the peripheral nervous system have been reported to be induced in rabbits (sensitization with GM1, BBG, or LPS) and rats (sensitization with SGPG; Saida et al, 1979;Maeda et al, 1991;Yamawaki et al, 1996;Yuki et al, 2001Yuki et al, , 2004. Kusunoki et al (1996) also reported a model for experimental sensory neuropathy induced by sensitization of rabbits using purified GD1b.…”

Anti-peripheral nerve myelin antibodies in Guillain-Barre syndrome bind a neutral glycolipid of peripheral myelin and cross-react with Forssman antigen.

“…Previous studies did not show in a consistent manner antibodies to any PNM component (27,28), even though both proteins and lipids known to induce inflammatory demyelination in experimental animals such as P2 and galactocerebroside (18,19) were included as antigens. In view of the finding that complement fixing Ab that react to normal PNM are consistently present in acute-phase GBS serum (5, 6), we wanted to know the specific antigen(s) of PNM that these anti-PNM Ab reacted to, as well as the heterogeneity of their reactivity.…”

“…Serum of these patients demyelinate cat sciatic nerve in the presence of complement (17). P2 and galactocerebroside both induce experimental neuritis in rats and rabbits (18,19). Ab to P2 a basic protein which is not exposed on the myelin surface does not demyelinate explants in vitro (20) while Ab to the surface determinant galactocerebroside causes in vivo and vitro demyelination (21,22) and mediates cytoxicity of Schwann cells (23).…”

Selective Vulnerability of Peripheral Nerves in Avian Riboflavin Deficiency Demyelinating Polyneuropathy

“…Demyelinative changes in both peripheral nerves and spinal nerve roots have also been reported in hypertrophic hereditary motor and sensory neuropathy, 4 protein zero-deficient mice, 9,26 peripheral myelin protein-22 deficient mice, 40 Trembler mice, 2 and Trembler-J mice 13 and in animal models of inflammatory demyelinating neuropathy. 1,14,17,24,38,39 In 2 mice with POEMS, which is a monoclonal plasma cell disorder characterized by polyneuropathy (P), organomegaly (O), endocrinopathy (E), monoclonal gammopathy (M), and skin changes (S), spinal nerve roots and sural nerves showed the same pathologic changes of demyelination, remyelination, and inflammatory cell infiltration, 42,47 and in 3 cases of diabetic neuropathy, there was severe loss of both large and small MF in sural nerves while segmental demyelination and remyelination was the main finding in both dorsal and ventral spinal roots. 32 Distal intramuscular and subcutaneous MF have rarely been examined in demyelinating peripheral neuropathies, although skin biopsy has been used in the diagnosis of disorders involving unmyelinated 21 and myelinated 11,23,25 fiber disorders.…”