Abstract
BackgroundThe 16/6-idiotype (16/6-Id) of the human anti-DNA antibody was found to induce experimental lupus in naïve mice, manifested by production of autoantibodies, leukopenia and elevated inflammatory markers, as well as kidney and brain involvement. We assessed behavior and brain pathology of naive mice injected intra-cerebra-ventricularly (ICV) with the 16/6-Id antibody.MethodsC3H female mice were injected ICV to the right hemisphere with the human 16/6-Id antibody or commercial human IgG antibodies (control). The mice were tested for depression by the forced swimming test (FST), locomotor and explorative activity by the staircase test, and cognitive functions were examined by the novel object recognition and Y-maze tests. Brain slices were stained for inflammatory processes.Results16/6-Id injected mice were cognitively impaired as shown by significant differences in the preference for a new object in the novel object recognition test compared to controls (P = 0.012). Similarly, the preference for spatial novelty in the Y-maze test was significantly higher in the control group compared to the 16/6-Id-injected mice (42% vs. 9%, respectively, P = 0.065). Depression–like behavior and locomotor activity were not significantly different between the16/6-Id-injected and the control mice. Immunohistochemistry analysis revealed an increase in astrocytes and microglial activation in the hippocampus and amygdala, in the 16/6-Id injected group compared to the control.ConclusionsPassive transfer of 16/6-Id antibodies directly into mice brain resulted in cognitive impairments and histological evidence for brain inflammation. These findings shed additional light on the diverse mosaic pathophysiology of neuropsychiatric lupus.See related Commentary article: http://www.biomedcentral.com/1741-7015/11/91
Highlights
The 16/6-idiotype (16/6-Id) of the human anti-DNA antibody was found to induce experimental lupus in naïve mice, manifested by production of autoantibodies, leukopenia and elevated inflammatory markers, as well as kidney and brain involvement
In the present study we investigated the effect of 16/6-Id on behavioral and cognitive functions, as well as on the brain pathology of naïve mice injected intra-cerebra -ventricularily (ICV) with the 16/6-Id
Cognitive and behavioral performance The results of cognitive performance in the novel object recognition test are presented as the proportion time spent near objects in both groups (Figure 1)
Summary
The 16/6-idiotype (16/6-Id) of the human anti-DNA antibody was found to induce experimental lupus in naïve mice, manifested by production of autoantibodies, leukopenia and elevated inflammatory markers, as well as kidney and brain involvement. Due to the varied diagnostic criteria applied to define NPSLE, the American College of Rheumatology has example, cytokines, matrix metalloproteinases), neuropeptides and endocrine factors [7,8,9,10] Other factors, such as medications and primary neurologic and psychiatric disorders, may play a major role as well. A wide profile of mice autoantibodies (for example, mouse 16/6Id, and antibodies against dsDNA, ssDNA, Ro, La, RNP, Sm, histones, cardiolipin and phosphatydilserine), were detected, as well as leukopenia, elevated erythrocyte sedimentation rate (ESR), proteinuria and the deposition of immunoglobulins in the kidney mesangium [30,31,32]. In the present study we investigated the effect of 16/6-Id on behavioral and cognitive functions, as well as on the brain pathology of naïve mice injected intra-cerebra -ventricularily (ICV) with the 16/6-Id
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