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Published on: June 29, 2015
Autoreactive antibodies against neurons and basal lamina found in serum following experimental brain contusion in
S Rudehill1, S Muhallab, A Wennersten
1Department of Clinical Neuroscience, Section of Neurosurgery, Karolinska Institute, Stockholm, Sweden.
Background:
Brain trauma is a risk factor for delayed CNS degeneration which may be attenuated by anti-inflammatory treatment. CNS injuries may cause anti-brain reactivity. This study was undertaken to analyze the pattern of delayed post-traumatic anti-brain immunity in experimental brain contusion.
Method:
Adult Sprague-Dawley and Lewis rats were subjected to experimental brain contusions. For B-cell investigations, serum was obtained from contused, control and naïve rats, and used for immunohistochemistry on slices of rat brains to first detect autoreactive IgG and IgM antibodies in rat serum. Secondly, anti-rat IgG and IgM antibodies were used to search for auto-antibodies already bound to the brain tissue. Double staining with rat-serum and NeuN or anti-GFAP antibody was used to detect anti-neuronal and anti-astrocytic antibodies, respectively. For T-cell reactivity, cells from brains and cervical lymph nodes of rats were used in FACS analysis and elispot with MBP and MOG stimulation.
Findings:
Anti-vascular basal lamina IgG antibodies were detected at three months in 6/8 rats, following experimental contusion. Anti-neuronal IgG antibodies were detected 2 weeks after experimental contusion and sham surgery, while naïve controls were negative. Individual rats showed a prolonged response, or an anti-astrocytic staining. Tissue bound anti-self IgG or IgM was not detected in the brain tissue. Anti-MBP or anti-MOG T-cell responses were not detectable.
Conclusions:
Experimental brain trauma and to some degree even sham surgery lead to an individually variable pattern of specific anti-brain reactive B-cells, while a T-cell response did not seem to be a consequence of moderate experimental contusion. The mere presence of anti brain-antibodies may be epiphenomenal, but could also be pathogenic for delayed degeneration. It is reasonable to regard the presence of an actual anti-brain reactivity as a potential threat to brain tissue integrity.
