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Modification of acute experimental autoimmune encephalomyelitis in the Lewis rat by oral administration of type 1 interferons. J Interferon Cytokine Res 1995 Feb;15(2):115-22

Date

02/01/1995

Pubmed ID

8590314

DOI

10.1089/jir.1995.15.115

Scopus ID

2-s2.0-0028964995 (requires institutional sign-in at Scopus site)   38 Citations

Abstract

The effect of orally administered type 1 interferons on the severity of acute experimental autoimmune encephalomyelitis (EAE), a T cell-mediated autoimmune disease, was examined by inoculation of Lewis rats with guinea pig myelin basic protein (GPMBP) and complete Freund's adjuvant. Rats were fed either rat species-specific or human recombinant type 1 interferon (IFN) or mock IFN daily for 7 days preceding immunization and for 21 days thereafter. There was a significant decrease in the clinical score and inflammatory foci in animals fed 5000 units IFN compared with mock-treated animals. There was a significant decrease in clinical score and number of inflammatory foci in spinal cord in animals fed orally 5000 units human recombinant IFN-alpha PO compared with SC 5000 units recombinant human IFN-alpha. Oral administration of type 1 interferon, as opposed to subcutaneous administration, inhibited the secretion of IFN-gamma from ConA-activated draining popliteal lymph node cells compared with mock-fed animals. These experiments demonstrate that acute EAE is more effectively inhibited by equivalent amounts of orally in contrast to parenterally administered IFN-alpha. These results suggest that type 1 IFNs are active by the oral route and have significant clinical and histologic effects in acute autoimmune disease.

Author List

Brod SA, Scott M, Burns DK, Phillips JT



MESH terms used to index this publication - Major topics in bold

Administration, Oral
Animals
Cells, Cultured
Concanavalin A
Encephalomyelitis, Autoimmune, Experimental
Female
Freund's Adjuvant
Guinea Pigs
Interferon Type I
Interferon-alpha
Interferon-beta
Interferon-gamma
Lymph Nodes
Lymphocyte Activation
Myelin Basic Protein
Rats
Rats, Inbred Lew
Recombinant Proteins
Spleen