Allergic Encephalomyelitis: Effect of Complement Depletion with Cobra Venom 1

Conclusion and Summary

Complement depletion of rats by cobra venom factor had only minor and variable effects on the hyperacute form of EAE. It appears likely that the exudation of polymorphonuclear leukocytes and massive amounts of fibrin in this condition is not dependent on complement. However, it is not possible to eliminate all traces of complement with cobra factor. Therefore, it is theoretically possible that small amounts of complement, too little to be detected by hemolytic activity or gel diffusion, might accumulate in the EAE lesions during the 1- to 3-day period in which they evolved. However, inhibition of the neutrophil accumulation of nephrotoxic serum glomerulitis attested to the efficacy of the cobra factor. This internal control provided evidence against the binding of C3 and terminal components, at least for the last 3 hr of development of EAE lesions. As C3 levels fall within 4 hr of the initial injection, it is most probable that complement depletion spanned the time during which EAE lesions developed.

Passive transfer of EAE can be accomplished in a single day. The rapidity of lesion development makes it highly likely that there was effective depletion of complement during the entire disease. Nevertheless, complement depletion of recipients had little or no effect on the outcome, either in conventional passive EAE in which mononuclear cells predominate or in the new, neutrophilic variety in which polymorphonuclear leukocytes are prominent.