Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of the heterodimeric complex of the calcium-binding proteins MRP-8 and MRP-14 was investigated in various inflammatory dermatoses using immunohistochemical staining with the monoclonal antibody 27E10. In addition to the inflammatory infiltrate, a positive staining was repeatedly found in the involved epidermis from patients with lichen planus, lupus erythematosus and psoriasis vulgaris, but not in normal skin epidermis and/or in epidermis from leucocytoclastic vasculitis patients. The keratinocytic expression of the 27E10 antigen was dissimilar to that of the MHC class-II molecules and the adhesion molecule ICAM-1. These data indicate that the 27E10 antigen is a distinct activation marker of inflammatory keratinocytes and may have proinflammatory properties.
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PMID:Epidermal expression of the calcium binding surface antigen 27E10 in inflammatory skin diseases. 128 18

To clarify the role of endothelial cells in the pathogenesis of vasculitis affecting peripheral nerve and skeletal muscle, the endothelial expression of adhesion molecules and major histocompatibility antigens (MHC) in different vasculitic syndromes were studied, and related to the presence of anti-endothelial cell antibodies (AECA). Increased expression of the intercellular adhesion molecule ICAM-1 in vasculitic lesions in nerve and muscle was shown, and this was associated with increased expression of MHC class I and II antigens. AECA were detected in low titre in only a minority of patients. The findings suggest that endothelial cells have a critical role in mediating the tissue injury in vasculitis affecting nerve and muscle and that the process is triggered by cellular and not antibody-mediated mechanism in the majority of patients.
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PMID:Endothelial cell activation in vasculitis of peripheral nerve and skeletal muscle. 137 48

The participation of leukocytes in the development of vascular disorders has been observed under various circumstances. Leukocyte activation occurs in extracorporeal blood circulation which lead to a pulmonary vascular sequestration and respiratory distress syndrome. Leukocytes could act on vascular components through at least two different pathways by releasing free oxygen radicals and proteases or by producing mediators such as interleukin 1, Tumor necrosis alpha, leukotrienes. Monocytes macrophages are present in the vascular wall at a very early stage of atherosclerosis. A majority of foam cells have been identified as macrophages loaded with lipids. Lymphocytes and monocytes are present in the atherosclerotic plaque. Leukocytes are also observed in the inflammatory lesion of vasculitis and experimentally activated lymphocytes can induce vasculitis. The molecular bases of leukocyte-endothelium interactions have been determined, and imply specialized molecules. Leukocyte Adhesion Molecule (LeucAM) appear to play a crucial role in leukocyte adhesion. On the endothelial cell side, endothelial cell adhesion molecule, intercellular adhesion molecule are receptors for leukocytes adhesion. They have been recently fully characterized. The better knowledge of leukocyte-vascular wall interactions offers new possible target for therapeutic agents.
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PMID:[Leukocytes and vascular lesions]. 204 28

Vascular endothelial cells respond in vitro to a number of stimuli, and in particular to cytokines, by undergoing functional and morphological alterations which endow them with the capacity to promote inflammatory reactions. We studied this process of endothelial cell activation in 20 skin biopsies from 18 patients with systemic vasculitis. At sites of cutaneous inflammation, blood vessels were lined with swollen endothelial cells which expressed increased levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and were associated with a mononuclear cell inflammatory infiltrate. Neutrophil infiltration was only found in the presence of endothelial leucocyte adhesion molecule-1 (ELAM-1), which was expressed in 15/20 biopsies. ELAM-1 and VCAM-1 were associated with the presence of inflammatory cytokines which induce expression of these molecules in cultured endothelial cells. Endothelial activation in vivo appears to parallel that observed in vitro, and is likely to be important in determining the nature of an inflammatory response.
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PMID:Endothelial cell activation in patients with systemic vasculitis. 753 91

The aim of this study was to investigate whether levels of circulating adhesion molecules reflect vascular inflammation in rheumatoid vasculitis (RV). Levels of circulating intercellular adhesion molecule-1 (cICAM-1), c-ICAM-3 and circulating endothelial leucocyte adhesion molecule (cE-selectin) were determined in 14 patients with RV and compared to 47 patients with rheumatoid arthritis (RA) and 100 healthy donors (HD). Enzyme-linked immunosorbent assays were used to quantify cICAM-1, cICAM-3 and cE-selectin. We found that in RV significantly (P < 0.0001) elevated levels of cICAM-1 and cICAM3, but not cE-selectin, were found when compared with RA patients. Levels > 2 S.D. above the mean level of HD were present for cICAM-1, cICAM-3 and cE-selectin in 57, 71 and 21%, respectively of patients with RV and 2, 21 and 44%, respectively of the RA patients. Increased levels of both cICAM-1 and cICAM-3 were found in 43% of the RV patients and in none of the RA patients. Comparison of the serum levels of patients studied in an active and inactive phase of RV revealed significantly lower levels of cICAM-3 levels in the inactive phase. In conclusion we find that determination of cICAM-1 and cICAM-3 may be useful as a marker of vascular inflammation in patients with RV.
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PMID:Levels of circulating intercellular adhesion molecule-1 and -3 but not circulating endothelial leucocyte adhesion molecule are increased in patients with rheumatoid vasculitis. 754 Apr 79

During inflammation, activated vascular endothelial cells and other cell types express various adhesion molecules which facilitate binding of circulating leukocytes. Serum concentration of circulating adhesion molecule ICAM-1 (c-ICAM-1) is supposed to reflect the degree of this activation. In order to evaluate the usefulness of c-ICAM-1 serum levels for assessment of disease activity in various vasculitic disorders, we examined 23 patients with systemic lupus erythematosus (SLE, n = 9). Wegener's granulomatosis (WG, n = 6), Goodpasture syndrome (GP, n = 6) and microscopic polyarteritis (MP, n = 2). Disease activity was defined by clinical criteria and by conventional laboratory data. Circulating ICAM-1 concentrations were measured during periods of active clinical vasculitis and on clinical remission. In a second part of the study, we examined whether or not c-ICAM-1 might be helpful in diagnosing acute allograft rejection early after kidney transplantation. After cadaveric kidney transplantation thirteen patients were included. Serum probes were gathered firstly after transplantation, secondly at time of histologically proven allograft rejection and finally after successful anti-rejection therapy and restored transplant function. c-ICAM-1 levels in healthy volunteers (n = 10) were 270 +/- 47 ng/ml (mean +/- SD). Patients with active vasculitis had mean serum levels of 509 +/- 71 ng/ml (SLE), 594 +/- 118 ng/ml (WG), 472 +/- 126 ng/ml (GP) and 498 ng/ml (MP) (mean +/- SD). In clinical remission, mean serum concentrations were found to be 500 +/- 99 ng/ml (SLE), 597 +/- 84 ng/ml (WG), 782 +/- 163 ng/ml (GP) and 594 ng/ml (MP) (mean +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum circulating ICAM-1 levels are not useful to indicate active vasculitis or early renal allograft rejection. 788

Neutrophils and monocytes (phagocytes) are important mediators of injury in many inflammatory diseases, including glomerulonephritis and vasculitis. Current treatment modalities (eg, corticosteroids, cytotoxic agents) are relatively nonspecific in their actions, frequently ineffective, and often associated with immunologic or metabolic complications. Recent advances in cellular and molecular immunobiology have suggested novel targets for therapeutic intervention. Phagocyte adhesion to endothelial cells, in particular, is a central event in the recruitment of phagocytes to sites of inflammation. Phagocyte trafficking to the extravascular space requires the coordinated interactions of several families of adhesion molecules, including the selectins, integrins, and immunoglobulin-like molecules. Initial attachment appears to be achieved by the interaction of phagocyte or endothelial cell selectins with carbohydrate-containing counter-receptors. These events facilitate immobilization of phagocytes via the interaction of phagocyte integrins with immunoglobulin-like molecules on endothelial cells and diapedesis to the extravascular tissue. Chemoattractants and cytokines regulate adhesion by altering the avidity or surface expression of preformed molecules and by influencing de novo synthesis of adhesion molecules. The intensity and composition of leukocyte infiltrates at sites of inflammation likely reflect the local balance of pro- and anti-inflammatory chemoattractants and cytokines and the profile of adhesion molecules on invading and resident cells. Adhesion may also promote tissue injury by augmenting phagocyte oxidative bursts and lysosomal enzyme release and by facilitating release of these cytotoxic molecules in close proximity to tissue cells. In addition, adhesion may amplify the levels and types of inflammatory mediators within a local milieu by promoting transcellular eicosanoid biosynthesis during cell-cell interaction. Increased adhesion molecule expression has been reported in glomerulonephritis, vasculitis, tubulointerstitial nephritis, transplant rejection, and hemodialysis "first-use" reactions. In addition, leukocyte adhesion may be an important event in the pathophysiology of ischemia-reperfusion injury. Monoclonal antibodies against adhesion molecules confer dramatic protection in several models of renal inflammation. Further studies in this area may yield potent and specific therapies for common renal diseases.
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PMID:Leukocyte adhesion molecules: potential targets for therapeutic intervention in kidney diseases. 792 75

Immunosuppressants are applied clinically on vasculitis. Cyclophosphamide, azathioprine, and methotrexate are used most often. Other immunosuppressants, such as bredinin, FK506, monoclonal antibody, and adhesion molecule are studied in laboratory level or in small group clinical trial. In combination therapy, immunosuppressants are used with corticosteroids, which are the first choice drug on angitis. Methotrexate is administered as intermittent manner. Since immunosuppressants have side effects including oncogenicity and immunotoxicity, clinicians have to pay much attention on clinical course of the patients with vasculitis.
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PMID:[Application of immunosuppressants for therapy of patients with vasculitis]. 793 8

Leukocyte binding to endothelial adhesion molecules has been said to be an initiating step in cardiac allograft rejection. Whether antibody blockage of leukocyte ligands, CD18, for intercellular adhesion molecule (ICAM-1) would prevent allograft rejection was studied in a rabbit heterotopic transplant model. Cervical cardiac transplant was performed between donor Staffland and New Zealand White recipient rabbits. Ten animals were treated with intravenous anti-CD8 monoclonal antibody, 60.3, at the dose of 1 mg/kg for 7 days. No immunosuppressive drugs were used. Eleven transplant controls were untreated. At 7 days, animals were sacrificed and donor heart histology was compared. Peripheral WBC counts were significantly higher in treatment group compared to untreated group on both postoperative day 2 and 7. The cellular rejection score was 30% lower in treated group than untreated (p < 0.05), demonstrating localization of lymphocytes to perivenular collections. The proportion of arteries with evidence of vasculitis was 45% lower in treated group. Results suggests that monoclonal antibody against LFA-1 (CD18) may hold promise as a therapeutic agent for both cellular and vascular rejection.
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PMID:[Monoclonal antibody against LFA-1 (CD18) inhibits cellular and vascular rejection in rabbit cardiac allografts]. 796 28

Vasculitis is a clinicopathologic process that involves inflammation and necrosis of blood vessels, resulting in a wide range of clinical diseases. The pathogenesis of vasculitis has been attributed to immunologic mechanisms, including immune complexes, cellular immunity, and humoral immunity, with numerous inciting events such as infection, drugs, malignancy, or toxins. Inflammatory cytokine production and adhesion molecule activation or upregulation are important determinants of the pathogenic inflammatory responses noted in vasculitis. Endothelial cells may be targeted by anti-endothelial cell antibodies and are central targets of numerous proinflammatory cytokines in vasculitis pathogenesis. Finally, antineutrophil cytoplasmic antibodies (ANCA) and T-cell responses to the protein targets of ANCA may play a role in vessel damage in ANCA-associated vasculitis.
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PMID:Changing concepts in pathophysiology of the vasculitides. 803 77


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