ABSTRACT
Objective Anti-ribosomal P antibodies (anti-P) are strongly associated with neuropsychiatric lupus. This study was designed to determine whether these antibodies are capable of causing electro-oscillogram (EOSG) and behavior alterations in rats. Methods IgG fraction anti-P positive and affinity-purified anti-P antibodies were injected intraventricularly in rats. Sequential cortical and subcortical EOSGs were analyzed during 30 days. IgG anti-Ro/SS-A and normal IgG were used as controls. Results All 13 animals injected with IgG anti-P demonstrated a high prevalence of polyspikes, diffusely distributed in hippocampal fields and cerebral cortex. These abnormalities persisted approximately a month. Remarkably, an identical electrical disturbance was observed with the inoculation of affinity-purified anti-P antibodies. The EOSG alterations were associated with behavioral disorders with varying degrees of severity in every animal injected with anti-P. In contrast, no changes in EOSG or behavioral disturbances were observed in the control group. Conclusion Our study indicates that anti-P antibodies can directly induce electrophysiological dysfunction in central nervous system particularly in hippocampus and cortex associated with behavior disturbances.
Subject(s)
Brain/physiopathology , Immunoglobulin G/administration & dosage , Lateral Ventricles/immunology , Lupus Erythematosus, Systemic/immunology , Mental Disorders/chemically induced , Ribosomal Proteins/immunology , Animals , Autoantibodies/administration & dosage , Autoantibodies/adverse effects , Brain/drug effects , Cerebral Cortex/drug effects , Cerebral Cortex/physiopathology , Disease Models, Animal , Female , Hippocampus/drug effects , Hippocampus/physiopathology , Humans , Immunoglobulin G/adverse effects , Injections , Lupus Erythematosus, Systemic/physiopathology , Male , Mental Disorders/physiopathology , RatsABSTRACT
A haemolytic assay was used to test the complement fixation ability of 16 serum samples with high concentrations of anti-cardiolipin antibodies. Fourteen patients had clinical complications usually associated with these antibodies--namely, recurrent abortions, thrombosis, or thrombocytopenia. Complement fixation by anticardiolipin antibodies was shown in only four of these patients and was not directly related to the antibody concentration. Because anticardiolipin antibodies in most of these patients did not activate the complement pathway it is unlikely that the complement cascade has an important role in the clinical complications associated with these antibodies.
