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Ingested interferon alpha induces Mx mRNA
1Department of Neurology and Graduate School of Biomedical Sciences, University of Texas-Houston, Houston, TX 77225, USA. sbrod@neuro.med.uth.tmc.edu
Abstract:
We have demonstrated that ingested murine interferon alpha (IFN-alpha) suppressed clinical relapse in chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE), decreased inflammation and suppressed the adoptive transfer of EAE, and is a biological response modifier in patients with multiple sclerosis. We examined the relative levels of the Mx mRNA signal using semiquantitative reverse transcription-polymerase chain reaction analysis on splenocytes from mice and peripheral blood mononuclear cells from man after IFN-alpha ingestion. Both mice and man demonstrated inducible levels of Mx mRNA after ingesting IFN-alpha. Murine spleen T cells and CD8(+)T cells also demonstrated upregulation of Mx mRNA. Murine whole splenocytes demonstrated upregulation of Mx mRNA after IFN-alpha ingestion of 10 and 100 U, but not after 0, 1000, 5000 U. Ingested IFN-alpha acts via established pathways of type 1 IFN signalling.
Insights
Ingested interferon alpha (IFN-alpha) effectively treats experimental autoimmune encephalomyelitis in mice by reducing inflammation and preventing relapse. This study confirms IFN-alpha
Area of Science:
- Immunology
- Neuroscience
Background:
- Interferon alpha (IFN-alpha) is a biological response modifier with potential therapeutic applications.
- Chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE) serves as a model for multiple sclerosis (MS).
Purpose of the Study:
- To investigate the molecular mechanisms underlying the therapeutic effects of ingested IFN-alpha in CR-EAE.
- To determine if ingested IFN-alpha induces a molecular response in both mice and humans.
Main Methods:
- Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze Mx mRNA levels.
- Splenocytes from mice and peripheral blood mononuclear cells (PBMCs) from humans were analyzed after IFN-alpha ingestion.
- Specific immune cell populations (T cells, CD8+ T cells) were examined in mice.
Main Results:
- Ingested IFN-alpha suppressed clinical relapse and inflammation in CR-EAE mice.
- Both mice and humans showed inducible levels of Mx mRNA after IFN-alpha ingestion.
- Murine spleen T cells and CD8+ T cells, as well as whole splenocytes, exhibited Mx mRNA upregulation at specific IFN-alpha doses (10 and 100 U).
Conclusions:
- Ingested IFN-alpha demonstrates therapeutic efficacy in a mouse model of MS.
- Mx gene induction by ingested IFN-alpha occurs in both mice and humans, suggesting conserved signaling pathways.
- The findings support the role of ingested IFN-alpha as a biological response modifier acting through type 1 interferon signaling pathways.