J Neuroimmunol 2003 Mar;136(1-2):94-103
Ledeboer A, Wierinckx A, Bol JG, Floris S, Renardel de Lavalette C, De Vries HE, van den Berg TK, Dijkstra CD, Tilders FJ, Van Dam AM.
Department of Medical Pharmacology, Research Institute Neurosciences, VU University Medical Center, Van der Boechorststraat 7, 1081 BT, Amsterdam, The Netherlands
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.