In vivo effect of sera from animals with chronic relapsing experimental allergic encephalomyelitis on central and peripheral myelin

Summary

Sera from guinea pigs with acute or chronic relapsing experimental allergic encephalomyelitis (EAE) were injected into the lumbosacral subarachnoid space of normal recipient rats. Seventeen of 37 sera induced demyelination in the CNS, and 27 of 37 sera caused demyelinated peripheral nerve fibers in the roots. The highest incidence of demyelinating activity of EAE sera was noted in those from donor animals sampled during the early chronic stage of the disease [40–100 days post sensitization (dps)]. Only few sera from animals sampled during the acute and subacute stage (10–40 dps) were able to induce demyelination. Sera from animals sampled between 100 and 200 dps showed a lower incidence of demyelinating activity as compared to those from the early chronic phase of the disease. There was no clear-cut correlation between the serum-demyelinating activity and the severity of the demyelinating disease in the donor animals. The patterns of demyelination in the central as well as peripheral nervous system of recipient animals were characterized by vesicular disruption of myelin or myelin stripping. Myelin degradation was performed mainly by macrophages. In the CNS some astrocytes also contained debris. Astrocytes increased in size, and mitosis of astrocytes was observed. Oligodendrocytes appeared to be unaffected. No demyelination was found when the sera from animals sensitized with CFA alone or with guinea pig liver tissue were injeted into the subarachnoid space of normal recipient rats.

Two possible mechanisms of demyelination are diseussed: Antibody-mediated complement-dependent and antibody-dependent cell-mediated demyelination.