Regional and temporal expression patterns of interleukin-10, interleukin-10 receptor and adhesion molecules in the rat spinal cord during chronic relapsing EAE

Annemarie Ledeboer, Anne Wierinckx, John G. J. M. Bol, Sarah Floris, Chantal Renardel de Lavalette, Helga E. de Vries, Timo K. van den Berg, Christine D. Dijkstra, Fred J. H. Tilders, Anne-Marie van Dam

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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 languageEnglish
Pages (from-to)94-103
Number of pages10
JournalJournal of neuroimmunology
Volume136
Issue number1-2
DOIs
Publication statusPublished - 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
  • Male
  • Multiple Sclerosis, Relapsing-Remitting
  • RNA, Messenger
  • Rats
  • Rats, Inbred Strains
  • Reaction Time
  • Receptors, Interleukin
  • Receptors, Interleukin-10
  • Spinal Cord
  • Time Factors
  • Vascular Cell Adhesion Molecule-1
  • Journal Article
  • Research Support, Non-U.S. Gov't

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