Expression of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in the spinal cord of
M Matsuda1, N Tsukada, C S Koh
1Department of Medicine (Neurology), Shinshu University, School of Medicine, Matsumoto, Japan.
Insights
Increased expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) in the rat central nervous system during EAE correlates with disease progression. These molecules may facilitate lymphocyte entry into the CNS, contributing to disease severity.
Area of Science:
- Neuroimmunology
- Cellular and Molecular Neuroscience
Background:
- Experimental allergic encephalomyelitis (EAE) is a model for multiple sclerosis.
- Cellular adhesion molecules play critical roles in immune cell trafficking.
Purpose of the Study:
- To investigate the expression of ICAM-1 and LFA-1 in the CNS during EAE.
- To correlate ICAM-1 and LFA-1 expression with disease progression.
Main Methods:
- Immunohistochemical analysis of ICAM-1 and LFA-1 expression in Lewis rat CNS during EAE.
- Correlation of cellular adhesion molecule expression with clinical and histopathological findings.
Main Results:
- ICAM-1 expression increased on endothelial cells in the CNS during active EAE, preceding clinical symptoms.
- LFA-1 was detected on perivascular infiltrating cells.
- Upregulation of ICAM-1 and LFA-1 showed an ascending pattern in the spinal cord, correlating with neurological signs.
- Peak expression occurred around the onset of clinical symptoms.
Conclusions:
- Increased ICAM-1 and LFA-1 expression in the CNS during EAE is an early event.
- These molecules likely contribute to lymphocyte extravasation across the blood-brain barrier.
- ICAM-1 and LFA-1 expression are associated with the progression of neurological deficits in EAE.
Abstract:
We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) by cells in the central nervous system (CNS) of Lewis rats during acute experimental allergic encephalomyelitis (EAE). A few endothelial cells in the CNS of normal rats expressed ICAM-1, whereas during the active phase of EAE, ICAM-1 was present on many endothelial cells. This alteration was detectable the day before clinical symptoms. Since histopathological studies showed few detectable mononuclear cells or inflammatory foci in any section of the preclinical rats, the expression of ICMA-1 was considered to be important at least in the early stage of inflammation. LFA-1 was seen on perivascular infiltrating cells. An increase in either ICAM-1- or LFA-1-positive cells was initially seen in the lumbosacral portion of the spinal cord, which then extended to the thoracic portion. The number of either ICAM-1- or LFA-1-positive cells peaked on the day of clinical onset in the lumbosacral portion. In contrast, in the thoracic portion, a peak in the number of either ICAM-1- or LFA-1-positive cells was observed on the day after clinical onset. This ascending extension of either ICAM-1- or LFA-1-positive cells was correlated with the progression of neurologic signs. It is suggested that increased expression of ICAM-1 and LFA-1 in the CNS of rat EAE may promote the extravasation of lymphocytes across the blood-brain barrier and be related to progression of the disease.
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