Cyclosporin-A treatment of experimental allergic encephalomyelitis: changes in immunological regulation and blood-CSF barrier function.
Strain 13 guinea pigs at 18-21 days of age were sensitised with spinal cord and Freund's complete adjuvant to induce experimental allergic encephalomyelitis (EAE). Treatment with cyclosporin-A (CS-A) from one day before sensitisation until from 12 to 39 days after sensitisation resulted in a suppression of the disease. Suppression was indicated by an absence or reduction in severity of clinical signs together with a lack of increase in blood-cerebrospinal fluid (CSF) barrier permeability to proteins and a lower white cell count in the CSF from treated animals. When CS-A treatment was withdrawn, clinical disease reappeared but changes in IgG concentration in the CSF indicated that intrathecal synthesis of IgG had occurred, which was not the case in the untreated disease. Modification by CS-A of the immunoregulatory processes involved in the development of EAE, provides a model to study the special conditions which operate in neuroimmunological disorders.
D000418:Albumins / Q000134:cerebrospinal fluid; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects; D002555:Cerebrospinal Fluid / Q000276:immunology / Q000473:pathology; D003524:Cyclosporins / Q000627:therapeutic use*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D006168:Guinea Pigs; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D013997:Time Factors
D000418:Albumins; D003524:Cyclosporins; D007074:Immunoglobulin G