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Query: UMLS:C0027121 (myositis)
4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interactions between leucocytes and endothelial cells through specific adhesion receptors play an increasingly recognized crucial role in the development of inflammatory infiltrates in chronic inflammatory diseases. In this study we investigated adhesion molecule expression in muscle biopsies from 18 dermatomyositis, six polymyositis, five inclusion-body myositis patients and from eight normal controls. Immunohistochemical detection of leucocyte integrins LFA-1 and VLA-4, their endothelial counter-receptors intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the endothelial cell markers CD31 and von Willebrand factor-related antigen (vWFAg) was performed using specific MoAbs and an alkaline phosphatase anti-alkaline phosphatase technique. ICAM-1 expression was up-regulated and VCAM-1 induced in muscle capillaries of dermatomyositis samples. In both dermatomyositis and polymyositis, endothelial cells from vessels surrounded by inflammatory infiltrates strongly expressed ICAM-1 and VCAM-1. Infiltrating leucocytes were intensively LFA-1- and VLA-4-positive. These data suggest that leucocyte/endothelial cell interactions mediated by the receptor/ligand pairs LFA-1/ICAM-1 and VLA-4/VCAM-1 actively participate in the development of muscle inflammatory infiltrates in the major inflammatory myopathies. In addition, ICAM-1 and VCAM-1 over-expression by capillary endothelial cells in dermatomyositis supports the hypothesis that capillary activation and/or injury is a major feature in this disease.
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PMID:Leucocyte/endothelial cell adhesion receptors in muscle biopsies from patients with idiopathic inflammatory myopathies (IIM). 909 32

Experimental allergic myositis (EAM) in Lewis rats, induced with partially purified myosin, is regarded as a model of human polymyositis. To clarify the role of adhesion molecules in the pathogenesis of EAM in Lewis rats, we investigated intramysial expressions of the intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, and the serum level of soluble ICAM-1 in EAM rats. All the EAM rat muscles had scattered inflammatory foci, as well as cell infiltration and necrosis, by week 4 after the initial immunization (i.e., day 0 after the last immunization). As compared with the control muscles, ICAM-1 and VCAM-1 were strongly expressed immunohistochemically in the endothelium of vessels in the endomysium and perimysium, and to lesser extents in the inflammatory infiltrates and on the sarcolemma of nonnecrotic muscle fibers adjacent to the inflammatory infiltrates or invaded muscle fibers. ICAM-1 in the muscle extracts and sera from EAM rats increased on each test day, as compared with extracts from the normal controls. The values peaked on day 0 after the last immunization, then gradually decreased with time. ICAM-1 elevations in the muscle extracts were correlated with the percent of sections that had inflammatory lesions (P = 0.032) and the histological scores (P = 0.005) on day 0, whereas there was no significance on days 3 and 7. These findings suggest that the adhesion molecules ICAM-1 and VCAM-1 increase in the early stage of EAM, and function in the initiation of the inflammatory process of myositis.
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PMID:Adhesion molecule expression in experimental myositis. 1187 Jul 19