Journal of Neuroimmunology, Vol. 129 (1-2) (2002) pp. 1-9
K. Schaecher 1 , A. Rocchini, J. Dinkins, D.D. Matzelle and N.L. Banik
Department of Neurology, Medical University of South Carolina (MUSC), Box 250606, Suite 307, 96 Jonathan Lucas Street, Charleston, SC 29425, USA
Calpain activity and expression at the protein level were examined in inflammatory cells, activated microglia, and astrocytes prior to or at onset of symptomatic experimental allergic encephalomyelitis (EAE), an animal model for the human demyelinating disease multiple sclerosis (MS).
EAE was induced in Lewis rats by injection of guinea pig spinal cord homogenate and myelin basic protein (MBP) emulsified with Complete Freund's Adjuvant (CFA).
Calpain translational expression, determined by Western blot and immunocytochemistry, was correlated with calpain activity, infiltration of inflammatory cells, and myelin loss at 2-11 days following challenge with antigen.
Controls (CFA only) did not show any changes over time in these parameters and very few changes (CD11+ microglia/mononuclear phagocytes) were seen in either group from days 2 to 8 post-induction.
In contrast, from days 9 to 11, the animals that developed the disease (at least grade 1) demonstrated extensive cellular infiltration (CD4+, CD25+, and CD11+) as well as increased calpain expression (content) and activity.
This study demonstrates that cell infiltration and increased calpain activity do not begin in the CNS until the onset of clinical signs.
© 2002 Published by Elsevier Science B.V.