Demyelination in vivo by Guillain-Barré syndrome and other human serum

Serum from patients with acute inflammatory polyneuropathy (the Guillain-Barré syndrome, GBS) demyelinates peripheral nerves in vivo more intensely than control human serum. To clarify the processes leading to demyelination we injected rat sciatic nerves with serum from GBS and control subjects in the presence of complement and examined the sequential morphologic changes over 7 days. One day after injection, five of six GBS sera but none of seven control sera caused vesicular demyelination; 3-5 days after injection both GBS and control sera produced macrophage-mediated demyelination. These observations suggest that GBS serum can initiate acute myelin injury through a humoral mechanism that is disease associated. This response appears to be distinct from delayed cell-mediated serum-induced demyelination that is not disease specific.