Mild experimental autoimmune encephalitis as a tool to induce blood-brain barrier dysfunction.
The blood-brain barrier (BBB) serves as a border limiting access of immunoglobulins from the circulation into the brain. This becomes relevant when studying the pathogenesis of antibody-mediated autoimmune CNS disorders. Here, we characterized the BBB dysfunction in a model of mild experimental adoptive transfer autoimmune encephalomyelitis (AT-EAE). We show that large molecules can readily penetrate the BBB between days 3 and 7 after EAE-induction. This model may be valuable for studying putative pathogenic effects of immunoglobulins in the central nervous system.
Boettger
Michael K
MK
Department of Neurology, University of Würzburg, Josef-Schneider-Strasse 11, 97080 Würzburg, Germany. michael.boettger@mti.uni-jena.de
Weishaupt
Andreas
A
Geis
Christian
C
Toyka
Klaus V
KV
Sommer
Claudia
C
D000418:Albumins / Q000378:metabolism; D000818:Animals; D001812:Blood-Brain Barrier / Q000503:physiopathology*; D001835:Body Weight; D002199:Capillary Permeability; D002540:Cerebral Cortex / Q000503:physiopathology; D053331:Ectodysplasins / Q000378:metabolism; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000503:physiopathology*; D005070:Evans Blue; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D007150:Immunohistochemistry; D009043:Motor Activity; D051381:Rats; D011917:Rats, Inbred Lew; D012720:Severity of Illness Index; D013116:Spinal Cord / Q000503:physiopathology; D013997:Time Factors
D000418:Albumins; C506018:EDA protein, human; D053331:Ectodysplasins; D007074:Immunoglobulin G; D005070:Evans Blue