Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Epidermal expression of the calcium binding surface antigen 27E10 in inflammatory skin diseases. 128 18

Circulating soluble ICAM-1 (sICAM-1) isoforms are known to be elevated in inflammatory and autoimmune disorders (SLE, RA). A correlation between levels of circulating sICAM-1 and disease activity was described (5). In sera from 31 patients suffering from histologically confirmed Wegener's granulomatosis (WG) elevated levels of ICAM-1 were now detected in this primary systemic vasculitis. In generalized active disease circulating ICAM-1 levels were significantly higher when compared to remission and healthy control individuals. Sera from WG patients collected during intercurrent infections while on immunosuppressive drugs showed no elevation of circulating ICAM-1.
 ...
PMID:[Elevated serum levels of ICAM-1 in Wegener's granulomatosis]. 135 97

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.
 ...
PMID:Endothelial cell activation in vasculitis of peripheral nerve and skeletal muscle. 137 48

Several studies during recent years have demonstrated the potential for vascular smooth muscle cells (SMC) and dermal fibroblasts to participate in immune interactions such as antigen presentation and alloreactivity. The molecular interactions mediating lymphocyte adhesion to these mesenchymal cells have, however, not previously been characterized in detail. In the present study we demonstrate ICAM-1 (CD54) expression by cultured human SMC and its up-regulation by IL-1, IFN-gamma, and bacterial lipopolysaccharide. Monoclonal antibodies were used to define the molecular interactions in the adhesion of 51Cr-labelled T lymphoblasts to adherent SMC and fibroblasts. ICAM-1 appeared to mediate adhesion of T lymphocytes by binding to the beta 2-integrin CD11a/CD18 (LFA-1) expressed by the lymphoblasts. We present evidence for the involvement of at least three different mechanisms in the adhesion of activated T lymphocytes to cultured fibroblasts. It was found that beta 2-integrin-mediated interaction could only account for less than half of the binding activity. The remaining adhesion was partly mediated by beta 1-integrins, presumably via VLA-5 since an anti-VLA-5 antibody and an RGD-containing peptide blocked adhesion to the same degree. However, antibodies to beta 1-, beta 2-, and beta 3-integrin subunits added together only inhibited adhesion by approximately 50%. The residual adhesion could be blocked by inhibition of cell metabolism and was increased by stimulation of the lymphocytes with phorbol ester, suggesting involvement of other, as yet undefined, adhesion molecules. The molecular interactions between lymphocytes and mesenchymal cells demonstrated in this study may have implications in several inflammatory conditions such as vasculitis, atherosclerosis, and connective tissue diseases.
 ...
PMID:Adhesion of activated T lymphocytes to vascular smooth muscle cells and dermal fibroblasts is mediated by beta 1- and beta 2-integrins. 138 Jan 79

Extensive damage is thought to occur to endothelial cells in renal vasculitis and other glomerulopathies. The state of inflammation of these endothelial cells was investigated through the use of a panel of monoclonal antibodies (MAb) directed against thrombospondin (TSP), von Willebrand factor (vWF), integrins (alpha IIb beta 3, alpha v beta 3), CD36, and classical markers of inflammation (P-selectin, E-selectin, ICAM-1, VCAM). Results show that the anti-TSP MAb (LYP10) stains large areas of interstitium in focal sclerosis, vasculitis, membranous glomerulonephritis (GN), and diabetic GN but does not in normal kidney. In contrast, very limited areas are stained by LYP10 in minimal change nephropathy and Berger's disease. On paraffin-embedded specimens these areas stained by LYP10 appear edematous and early fibrous. Up-regulation of vWF and ICAM-1 is matched by an increased binding of LYP10 to the interstitium. In addition, fibrous crescents in injured glomeruli are stained by LYP10. This study reports for the first time an increased TSP secretion in glomerulopathies. Such TSP secretion may be part of physiological adaptive changes associated with inflammation and early fibrosis.
 ...
PMID:Thrombospondin in human glomerulopathies. A marker of inflammation and early fibrosis. 751 60

The adhesion molecules ICAM-1, VCAM-1 and E-Selectin are regulated by proinflammatory cytokines and play an important role in the binding and activation of leukocytes in inflammatory diseases. This study measured the serum concentrations of circulating adhesion molecules (cICAM-1, cVCAM-1, cE-Selectin) by sandwich ELISA in systemic vasculitis with renal involvement (Wegener's granulomatosis WG, n = 25; systemic lupus erythematosus SLE, n = 50) in comparison to chronic glomerulonephritis (n = 10), stable renal allograft function and end-stage renal disease (CAPD/hemodialysis, each n = 10). Both cICAM-1 and cVCAM-1 levels, but not cE-Selectin, were significantly increased (p < 0.001) in active WG compared to healthy controls. cICAM-1, not cVCAM-1 differed significantly between active and inactive WG. Only cVCAM-1 was significantly elevated in active/inactive SLE (p < 0.01). WG with rapidly progressive glomerulonephritis had significantly raised levels of cICAM-1 and cVCAM-1, but not cE-Selectin, compared to controls (p < 0.005). In lupus nephritis only cVCAM-1 was significantly elevated (p < 0.01). cICAM-1 and cVCAM-1 levels were significantly raised in WG patients, that were hemodialysed and in patients with hemodialysis because of different reasons when compared to controls. However, cVCAM-1 but not cICAM-1 was significantly higher in WG with HD than without HD. Patients with chronic glomerulonephritis, renal allografts or CAPD also had significantly raised cVCAM-1 concentrations. These data suggest, that levels of circulating adhesion molecules might reflect different pathophysiologic processes in systemic vasculitides and endothelial/immune activation in non-inflammatory renal diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Detection of circulating adhesion molecules ICAM-1, VCAM-1 and E-selectin in Wegener's granulomatosis, systemic lupus erythematosus and chronic renal failure. 754 87

Endothelial cell activation is achieved by the rapid, protein synthesis-independent induction of a characteristic set of genes. Because of the abundance of binding sites for the transcription factor NF-kappa B in the regulatory region of the aforementioned genes, we hypothesized that this factor might play a key role. Reactive oxygen intermediates act as second messengers in the activation of NF-kappa B. We have used the antioxidant pyrrolidine dithiocarbamate to analyze the effect of NF-kappa B inhibition on TNF alpha-induced EC activation in vitro. We show that pyrrolidine dithiocarbamate strongly reduces the TNF alpha-mediated induction of E-selectin, VCAM-1, ICAM-1, PAI-1, tissue factor, IL-8 and I kappa B-alpha. We present evidence identifying NF-kappa B as a central of EC activation. Therefore, this factor may represent a prime target for therapeutic intervention in pathologic conditions associated with EC activation such as allo- and xenograft rejection, atherosclerosis, ischemic reperfusion injury and vasculitis.
 ...
PMID:Inhibition of NF-kappa B by pyrrolidine dithiocarbamate blocks endothelial cell activation. 754 93

Rat kidneys were perfused with anti-intercellular adhesion molecule-1 (anti-ICAM-1) monoclonal antibody prior to allotransplantation. In the two strain combinations examined, LEF-to-WKAH transplants resulted in accelerated graft loss, and no prolongation of graft survival. The accelerated graft loss was the result of frequent occurrence of necrotizing arteritis within the grafts. In contrast, TO-to-WKAH transplants resulted in no change in graft survival and no arteritis. Necrotizing vasculitis in the LEJ-to-WKAH grafts was characterized by fibrinoid necrosis, collection of cellular infiltrates and serum macromolecular protein entrapment. The F(ab1)2 form of anti-ICAM-1 antibody partially preserved the antibody's capacity to accelerate graft loss. Therefore, although endothelial injury by Fc-mediated cytotoxicity may be involved in vascular damage, other mechanisms also come into play. The amount and distribution pattern of ICAM-1 antigen were identical in both TO and LEJ strains. Intravenous anti-ICAM-1 antibody administration combined with lipopolysaccharide, Poly(I)-Poly(C), warm ischemia to the kidney, or subcutaneous immunization with allogeneic spleen cells, but without renal transplantation, did not generate necrotizing vasculitis or proteinuria. These observations plus our previous data on the rat liver transplantation model clearly show that graft perfusion with anti-ICAM-1 monoclonal antibody invokes extensive vascular damage within allografts by Fc-mediated and Fc-independent mechanisms, depending on the donor-to-host combination.
 ...
PMID:Strain combination-dependent genesis of necrotizing arteritis in anti-ICAM-1 antibody-perfused renal allografts in the rat. 778 89

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)
 ...
PMID:Serum circulating ICAM-1 levels are not useful to indicate active vasculitis or early renal allograft rejection. 788

Intercellular adhesion molecule-1 (ICAM-1), a member of the immunoglobulin supergene family, is known to play an important role in inflammatory diseases. Using a previously developed enzyme-linked immunosorbent assay (ELISA) with two monoclonal antibodies (MoAbs) against human ICAM-1, levels of soluble ICAM-1 (sICAM-1) were measured in sera from patients with collagen diseases and in synovial fluids (SF) from patients with rheumatoid arthritis (RA). Although the results did not demonstrate that RA and other collagen diseases, as a group, had significantly higher levels of sICAM-1 in sera as compared with healthy controls, 21 of 138 cases (15%) with collagen diseases and 11 out of 57 patients (19%) with RA clearly showed higher levels of sICAM-1 in the sera. Comparisons between RA patients of radiological stages I and II and between stage I and other stages showed significantly higher levels of sICAM-1 in the sera of patients in the latter stages. RA patients with vasculitis and/or pneumonitis showed significantly higher levels of sICAM-1 than those without vasculitis or pneumonitis. Significant correlations were demonstrated between sICAM-1 and the factors IgG-RF, IgM-RF, erythrocyte sedimentation rate (ESR) and TNF-alpha in sera of RA patients. In addition, it was noted that the levels of sICAM-1 in SF were as high as those in the sera of patients with RA.
 ...
PMID:Soluble intercellular adhesion molecule-1 (ICAM-1) antigen in patients with rheumatoid arthritis. 790 95


1 2 3 4 5 6 Next >>