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Author (up) Agnello, D.; Bigini, P.; Villa, P.; Mennini, T.; Cerami, A.; Brines, M.L.; Ghezzi, P.
Title Erythropoietin exerts an anti-inflammatory effect on the CNS in a model of experimental autoimmune encephalomyelitis Type Journal Article
Year 2002 Publication Brain Research Abbreviated Journal
Volume 952 Issue 1 Pages 128-134
Keywords Animals; Anti-Inflammatory Agents/*pharmacology; Arthritis, Experimental/drug therapy/immunology; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental/*drug therapy/immunology; Erythropoietin/*pharmacology; Female; Interleukin-6/metabolism; Multiple Sclerosis/drug therapy/immunology; Rats; Rats, Inbred Lew; Research Support, Non-U.S. Gov't; Spinal Cord/immunology/metabolism; Tumor Necrosis Factor-alpha/metabolism
Abstract In recent work we reported that systemically administered erythropoietin (EPO) crosses the blood-brain barrier and has protective effects in animal models of cerebral ischemia, brain trauma and in a rat model of experimental autoimmune encephalomyelitis (EAE). Here we characterize the effect of systemic EPO on the inflammatory component of actively induced, acute EAE in Lewis rats. Administration of EPO at doses of 500-5000 U/kg bw i.p., daily from day 3 after immunization with myelin basic protein (MBP), delayed the onset of EAE and decreased its clinical score at peak time (days 12-13). Immunohistochemical analysis of the spinal cord using anti-glial fibrillary acidic protein (GFAP) and anti-CD11b antibodies showed that EPO markedly diminished inflammation and glial activation/proliferation. EAE induced significant levels of TNF and IL-6 in the spinal cord, where IL-6 was maximum at the onset of the disease (day 10) and TNF at its peak (day 12). EPO delayed the increase of TNF levels, without altering their peak levels, and markedly reduced those of IL-6 suggesting that the decreased inflammation and clinical score may be in part upon attenuation of IL-6. On the other hand, EPO was without effect in a model of adjuvant-induced arthritis in Lewis rats, suggesting a specificity towards autoimmune demyelinating diseases. These data suggest that EPO might act as a protective cytokine in inflammatory pathologies of the CNS.
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Notes 0006-8993 (Print) Journal Article Approved no
Call Number refbase @ admin @ Agnello2002 Serial 818
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