Experimental Research Autoreactive antibodies against neurons and basal lamina found in serum following experimental brain contusion in rats

Summary 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 na€ � ve 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. Antineuronal IgG antibodies were detected 2 weeks after experimental contusion and sham surgery, while na€ � ve 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 antibrain 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.