Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intercellular Adhesion Molecule-1 (ICAM-1) is a cytokine-inducible adhesion molecule expressed on cells of multiple lineages at sites of inflammation. Recently a truncated form of ICAM-1 has been discovered to be circulating in serum. This study reports on circulating serum (cICAM-1) levels in 132 uveitis patients (HLA-B 27 pos. acute anterior uveitis (AAU); HLA-B27 neg. anterior uveitis (AU); intermediate uveitis (IU); heterochromic cyclitis Fuchs (HCF); sarcoidosis; Toxoplasmosis). Measurement of circulating ICAM-1 serum levels was performed using a monoclonal antibody based ELISA, with healthy blood donors serving as the control group. Applying multiple variance analysis and the Student Newmann-Keuls test we found a statistically significant elevation of serum cICAM-1 level in the HLA-B 27 neg. AU group (n:31), in the IU group (n:25) and in patients with sarcoidosis (n:18). Serum levels of HLA-B27 pos. AAU patients, patients with HCF and patients suffering from ocular toxoplasmosis did not differ significantly from levels of the control group.
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PMID:Circulating ICAM-1 levels in serum of uveitis patients. 135 55

Adhesion molecules are known to be an important part of leukocyte migration and extravasation in both homeostatic and inflammatory conditions. Intracellular adhesion molecule-1 (ICAM-1 or CD54) is constitutively expressed on endothelial cells and is up-regulated during acute and chronic inflammation. We investigated the efficacy and consequences of interfering with CD54 after administration of an antisense oligonucleotide to ICAM-1 (CD54) in the transgenic HLA-B27/beta2 microglobulin rat model. One hundred percent of the HLA-B27 transgene + animals will spontaneously develop chronic inflammation (some more severely than others) in the gastric mucosa, cecum, and colon. We carried out two studies, i.p. injection and rectal administration of antisense. Following i.p. and rectal treatment, there were significant decreases in colonic mucosal wall thickness, histologic inflammation, CD54 expression in the colon and peripheral blood, and the percentage of colon weight per end body weight. Furthermore, decreased expression of CD49d, CD18, and tumor necrosis factor-alpha was observed in antisense treated rats. Therefore, the HLA-B27 transgenic model of spontaneous and chronic inflammatory bowel disease, which has increased expression of adhesion molecules, responds to both routes of administration of ICAM-1 antisense oligonucleotides. These studies support the regulatory role of adhesion molecules in chronic intestinal inflammation, the need for an understanding of how the route of drug delivery can alter the dose and area affected, and finally the role of antisense oligonucleotides as a therapeutic modality in chronic spontaneous inflammatory bowel diseases.
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PMID:Amelioration of chronic and spontaneous intestinal inflammation with an antisense oligonucleotide (ISIS 9125) to intracellular adhesion molecule-1 in the HLA-B27/beta2 microglobulin transgenic rat model. 1218 46