Soluble ICAM‐1 serum levels in multiple sclerosis and viral encephalitis

Abstract

Intercellular adhesion molecule ICAM-1 has a crucial role in the induction of an immune response and is instrumental in migration of T cells into inflamed tissue. We studied soluble ICAM-1 concentrations in patients with multiple sclerosis (MS), viral encephalitis, and other immunologic diseases, and compared results with those in other noninflammatory, nondemyelinating neurologic disorders as well as in healthy controls. MS patients with clinically active disease or enhancing lesions on MRI had elevated serum levels of soluble ICAM-1. Concentrations of soluble ICAM-1 were also increased in some patients with viral encephalitis. These findings raise the possibility that circulating ICAM-1 serves as a marker of acute inflammatory events in the brain and add to evidence implicating this adhesion molecule in the pathogenesis of MS.

Immunological monitoring of azathioprine treatment in multiple sclerosis patients

“…The levels of circulating sICAM-1 did not change during treatment. The serum sICAM-1 levels in MS are still controversial: while two studies [13,41] have detected higher levels in clinically active MS patients than in controls, another study [16] has failed to detect differences between clinically active MS and non-inflammatory immunological diseases. While these discrepancies may partly relate to the use of different kits for sICAM-1 quantitation, the low number of relapses in our patients precludes definite conclusions on this point.…”

“…Recently, serum and cerebrospinal fluid (CSF) circulating adhesion molecules, potentially released by activated blood or CSF cells or by CNS endothelial cells, have been suggested to be related to the clinical activity of MS [9,13].…”

“…Moreover, decrease in the percentage of peripheral blood "suppressor-inducer" (i.e. CD4 + CD45RA + ) T-lymphocytes has been reported, particularly in patients with progressive disease [22].Recently, serum and cerebrospinal fluid (CSF) circulating adhesion molecules, potentially released by activated blood or CSF cells or by CNS endothelial cells, have been suggested to be related to the clinical activity of MS [9,13].Abstract Despite the longstanding clinical use of azathioprine as an immunosuppressive agent in multiple sclerosis, little is known about the action of this drug on a number of parameters of putative pathogenic relevance in the disease. Eleven patients with multiple sclerosis, treated with azathioprine 2.5-3 mg/kg per day, and six untreated patients were studied with serial blood sampling for 1 year.…”

Transcriptional regulation of the intercellular adhesion molecule-1 gene by proinflammatory cytokines in human astrocytes

“…In Alzheimer's disease, ICAM-1 accumulates in senile plaques (Akiyama et al, 1993;Verbeek et al, 1994), and in patients with multiple sclerosis (MS), ICAM-1 expression is increased in brain lesions as well as on MS-derived brain microvascular endothelial cells (Sobel et al, 1990;Washington et al, 1994;Lou et al, 1997). In addition, increased levels of soluble ICAM-1 in the serum and cerebrospinal fluid of patients with active MS correlate with disease severity (Hartung et al, 1993;Sharief et al, 1993). The involvement of ICAM-1 in neurological disease has been further supported by recent studies in the EAE model and the Theiler's virus-induced demyelination model, in which administration of anti-ICAM-1 and anti-LFA-1 antibodies ameliorated disease progression, possibly by blocking T cell migration through the BBB (Inoue et al, 1997;Morrissey et al, 1996).…”

PECAM-1 (CD31) expression in the central nervous system and its role in experimental allergic encephalomyelitis in the rat

“…VLA-4 and LFA-1 are expressed on activated T lymphocytes and macrophages, while ICAM and VCAM are expressed de novo or are upregulated in EAE and MS brain tissues (Cannella et al, 1990;Wilcox et al, 1990;Cannella et al, 1991;Lassmann et al, 1991;O'Neill et al, 1991;Sobel et al, 1991;Archelos et al, 1993;Hartung et al, 1993;Washington et al, 1994;Cannella and Raine, 1995).…”