Abstract
Adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) mediate leukocyte infiltration into the CNS, in experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS). Because exogenous interleukin-10 (IL-10) inhibits ICAM-1 and VCAM-1 expression and clinical EAE, we hypothesize that endogenous IL-10 signaling may suppress expression of adhesion molecules. In a rat model of chronic relapsing EAE, expression levels of IL-10 and its receptor (IL-10R1), ICAM-1 and VCAM-1 mRNA in the spinal cord are markedly increased, whereas levels of IL-10 mRNA remain relatively low. The temporal pattern of mRNA and protein expression showed marked differences between spinal cord levels. During relapse, IL-10, IL-10R1, ICAM-1, VCAM-1 mRNA levels and neurological scores show positive correlations. We conclude that endogenous IL-10 is not a crucial factor inhibiting adhesion molecule expression in this model.
Original language | English |
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Pages (from-to) | 94-103 |
Number of pages | 10 |
Journal | Journal of Neuroimmunology |
Volume | 136 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - Mar 2003 |
Keywords
- Animals
- Cell Adhesion Molecules
- Chemotaxis, Leukocyte
- Chronic Disease
- Disease Models, Animal
- Encephalomyelitis, Autoimmune, Experimental
- Gene Expression Regulation
- Immunohistochemistry
- Intercellular Adhesion Molecule-1
- Interleukin-10
- Journal Article
- Male
- Multiple Sclerosis, Relapsing-Remitting
- RNA, Messenger
- Rats
- Rats, Inbred Strains
- Reaction Time
- Receptors, Interleukin
- Receptors, Interleukin-10
- Research Support, Non-U.S. Gov't
- Spinal Cord
- Time Factors
- Vascular Cell Adhesion Molecule-1