UMLS:C0001511 - FACTA Search

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Query: UMLS:C0001511 (Adhesion)
5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Leukocyte-endothelial cell interactions play an important role during ischaemia-reperfusion events. Adhesion molecules are specifically implicated in this interaction process. 2. Since defibrotide has been shown to be an efficient drug in reducing damage due to ischaemia-reperfusion in many experimental models, we analysed the effect of defibrotide in vitro on leukocyte adhesion to endothelial cells in basal conditions and after their stimulation. 3. In basal conditions, defibrotide (1000 micrograms ml-1) partially inhibited leukocyte adhesion to endothelial cells by 17.3% +/- 3.6 (P < 0.05), and after endothelial cell stimulation (TNF-alpha, 500 u ml-1) or after leukocyte stimulation (fMLP, 10(-7) M), it inhibited leukocyte adhesion by 26.5% +/- 3.4 and 32.4% +/- 1.8, respectively (P < 0.05). 4. In adhesion blockage experiments, the use of the monoclonal antibody anti-CD31 (5 micrograms ml-1) did not demonstrate a significant inhibitory effect whereas use of the monoclonal antibody anti-LFA-1 (5 micrograms ml-1) significantly interfered with the effect of defibrotide. 5. This result was confirmed in NIH/3T3-ICAM-1 transfected cells. 6. We conclude that defibrotide is able to interfere with leukocyte adhesion to endothelial cells mainly in activated conditions and that the ICAM-1/LFA-1 adhesion system is involved in the defibrotide mechanism of action.
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PMID:Drug-induced in vitro inhibition of neutrophil-endothelial cell adhesion. 876 67

The aim was to investigate circulating E-selectin and Intercellular Adhesion Molecule-1 (ICAM-1) in acute myocardial infarction. Our study was carried out in 80 patients, 40 hospitalized for acute myocardial infarction (AMI), 20 suffering from chronic stable angina and 20 healthy control subjects. Samples of venous blood were taken from all patients at the moment of hospitalization and after 2, 4, 6, 8, 10, 12 and 24 hours from the thrombolytic treatment (AMI + urokinase) or conventional therapy (AMI + nitroglycerin), for the dosage of creatinine kinase (CK) and adhesion molecules. The CK was determined by means of a Hitachi 901 automatic analyser using an enzymatic method (reagents Boheringer-Biochemia, Germany). Soluble E-selectin (sE-selectin) and soluble ICAM-1 (sICAM-1) were measured in the serum using a specific immunoassay (British Biotechnology Products). The serum levels of Tumor Necrosis Factor (TNF-alpha) were evaluated using an immunoenzymatic assay to quantitate the serum levels of the cytokine (British Biotechnology Products). Patients with acute myocardial infarction (AMI) had increased serum levels of soluble E-selectin (sE-selectin; AMI + urokinase = 312 +/- 20 ng/ml; AMI + nitroglycerin = 334 +/- 15 ng/ml) and soluble ICAM-1 (sICAM-1; AMI + urokinase = 629 +/- 30 ng/ml; AMI + nitroglycerin = 655 +/- 25 ng/ml) compared to both patients with chronic angina (sE-selectin = 67 +/- 10 ng/ml; sICAM-1 = 230 +/- 20 ng/ml) and healthy control subjects (sE-selectin = 53 +/- 15 ng/ml; sICAM-1 200 +/- 16 ng/ml). Furthermore patients with acute myocardial infarction also had increased serum levels of Tumor Necrosis Factor (TNF-alpha = 309 +/- 10 pg/ml; control subjects = 13 +/- 5 pg/ml). Thrombolytic therapy with urokinase (1,000,000 IU as an intravenous bolus for 5 minutes, followed by an infusion of an additional 1,000,000 IU for the following two hours) succeeded in producing reperfusion and reduced the serum levels of sE-selectin (52 +/- 13 ng/ml) and sICAM-1 (202 +/- 31 ng/ml). In contrast patients not eligible for thrombolytic therapy and therefore treated with conventional therapy (a continuous i.v. infusion of nitroglycerin at the dose of 50 mg/die) did not show any significant reduction in both sE-selectin and sICAM-1 throughout the study. Our results confirm previous experimental data and indicate that adhesion mechanisms supporting leukocyte-endothelium interaction may also be operative in human acute myocardial infarction.
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PMID:Thrombolytic therapy with urokinase reduces increased circulating endothelial adhesion molecules in acute myocardial infarction. 882 73

The infiltration of pancreatic islets by mononuclear cells is the hallmark of the development of insulin dependent diabetes mellitus (IDDM) in the NOD mouse, an animal model for human IDDM. The aim, of this study was to correlate adhesion molecule expression with the degree of islet infiltration and to compare Th1- and Th2-driven islet inflammation. Cryostat sections of NOD mouse pancreata before and after diabetes development were analysed by semiquantitative immunohistochemistry. NOD mouse islets did not show the expression of ICAM-1, LFA-1, L-selectin and VCAM-1 prior to infiltration by mononuclear cells. Furthermore, islets with early stage insulitis (grade 1, periinsular location of small infiltrates) still were devoid of adhesion molecule expression. ICAM-1 and LFA-1 were first demonstrable in islets with strong periinsular infiltrates (insulitis grade 2) while L-selectin and VCAM-1 were only seen in islets with mild or strong intraislet infiltration (grade 3-4). Adhesion molecules were demonstrable in areas of macrophage and T-lymphocyte infiltrates but not in adjacent endocrine islet tissue. Islets of all infiltration stages contained Th2 lymphocytes (positive for IL-4). Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.). Interestingly, the adhesion molecule expression pattern in islets with "Th1' versus "Th2 insulitis' was not different. In conclusion, the expression of adhesion molecules in islets during the development of autoimmune diabetes does not precede mononuclear infiltration but probably occurs in response to the activation of initial small infiltrates. ICAM-1 and LFA-1 expression is seen prior to L-selectin and VCAM-1. However, adhesion molecule expression during Th1 versus Th2 cell infiltration is very similar, suggesting similar adhesion molecule requirements of the two Th subsets.
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PMID:Differential expression of ICAM-1 and LFA-1 versus L-selectin and VCAM-1 in autoimmune insulitis of NOD mice and association with both Th1- and Th2-type infiltrates. 893 79

Coal workers' pneumoconiosis (CWP) is characterized by a chronic inflammatory lung reaction associated with macrophage accumulation in alveolar spaces. In this study, we investigated in CWP the implication of adhesion molecules such as E-selectin, ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) and the role of TNF-alpha which is one of the cytokines inducing their expression. Adhesion molecule expression was analysed by immunohistochemistry on lung biopsies from patients with CWP and from healthy subjects. In parallel, soluble adhesion molecules were detected in bronchoalveolar lavage fluids (BALF) from patients by specific ELISA. The involvement of TNF in the induction of these adhesion molecules was measured (i) by immunohistochemistry on sections from lung fragments, and (ii) by evaluating in vitro the expression of adhesion molecules on endothelial cells and on alveolar epithelial cells in the presence of alveolar macrophage supernatants. In control subjects, a weak staining of ICAM-1 was detected only in alveolar walls, while E-selectin and VCAM-1 were undetectable. In pneumoconiotic patients, ICAM-1 was expressed at a high level by endothelium, by alveolar and bronchial epithelial cells and by alveolar macrophages. E-selectin and VCAM-1 expression remained undetectable. Measurement of soluble adhesion molecule showed that only the concentration of sICAM-1 was significantly increased in BALF from patients with CWP compared with controls. The involvement of TNF in this ICAM-1 expression was shown by the in vitro effect of alveolar macrophage supernatants on adhesion molecule expression by endothelial cells and epithelial cells (this effect was neutralized by anti-TNF antibodies) and by the increased production of TNF in the lung of pneumoconiotic patients. These data provide evidence for the involvement of ICAM-1, induced at least in part by alveolar macrophage-derived TNF, in the development of the inflammatory reaction in CWP.
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PMID:Expression of leucocyte-endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-alpha). 897 25

This study examined the adhesive interactions of peripheral blood B cells with TNF-alpha-activated endothelial monolayers, and analyzed the roles of E-selectin, P-selectin, or VCAM-1 molecules expressed on activated HUVEC. B cell interaction occurred on activated HUVEC, but not on resting HUVEC under flow conditions. The majority of peripheral blood B cells expressed P-selectin glycoprotein ligand-1 and alpha4 integrin. However, the expression of cutaneous lymphocyte Ag on B cells was low. Under flow conditions, B cells could bind to P-selectin-coated tubes and VCAM-1-transfected Chinese hamster ovary cells. In contrast, B cells could not bind to E-selectin-coated tubes. Adhesion activity of B cells to P-selectin-coated tubes was weaker than that of T cells. Furthermore, adhesion activity of B cells to VCAM-1-transfected Chinese hamster ovary cells was similar to that of T cells. Treatment of activated HUVEC with anti-VCAM-1 mAb reduced interaction of B cells under flow conditions. However, the treatment of activated HUVEC with anti-P-selectin mAb did not reduce interaction. These data indicated that the interaction of VCAM-1 with alpha4 integrin plays a major role in an initial attachment of B cells to endothelial monolayers under flow conditions.
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PMID:Analysis of initial attachment of B cells to endothelial cells under flow conditions. 899 86

Major histocompatibility class II molecules (MHC class II), whose biosynthesis and expression by endothelial cells can be induced by gamma-interferon (IFN-gamma), play a major role in antigen recognition and subsequent cell-cell interactions involved in the initiation of immune responses. Adhesion molecules such as E-selectin and intercellular adhesion molecules (ICAM-1), whose biosynthesis and membrane expression by endothelial cells is regulated by proinflammatory cytokines (IL-1 and TNF), are necessary for the attachment and subsequent extravasation of leukocytes into the surrounding tissue. In the present study, the effects of preformed inflammatory mediators (histamine and serotonin) on the induction and expression of MHC class II, E-selectin, and ICAM-1 molecules by human umbilical vein endothelial cells were examined. Serotonin but not histamine was found to significantly inhibit in a dose-response fashion the induction and expression of MHC class II molecules. Inhibition occurred when it was added 24 h before, at the same time (most effective), or 24 h after IFN-gamma stimulation. No enhancement or stimulation of MHC class II biosynthesis could be detected using moderate or low concentration of either histamine or serotonin alone. In contrast to MHC class II molecules, neither serotonin nor histamine blocked the induction and biosynthesis of E-selectin and ICAM-1 molecules as detected by specific H18/7 and RR1/1 monoclonal antibodies, respectively, using flow cytometry. These findings suggest that serotonin but not histamine can assist in regulating the induction and expression of MHC class II molecules. Failure to block biosynthesis of E-selectin and ICAM-1 induced by TNF-alpha and IL-1 beta indicates the inhibitory effect exerted by serotonin was selective in nature.
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PMID:Differing regulation of major histocompatibility class II and adhesion molecules on human umbilical vein endothelial cells by serotonin. 903 94

This study examines the molecular mechanisms that underlie the observed preferential interactions of memory vs naive T cells with activated vascular endothelium. Many more CD4+ CD45RO+ (memory) cells adhered to 6-h TNF-alpha-activated human umbilical vein endothelium under flow than CD4+CD45RA+ (naive) cells. Adhesion studies were performed using Chinese hamster ovary (CHO) cell monolayers expressing human E- or P-selectin (CHO-E and CHO-P, respectively) or with soluble vascular cell adhesion molecule-1 (VCAM-1)-coated glass surfaces. Under flow at 1.8 dynes/cm2, RO+ T cells rolled extensively at low velocity on both CHO-P and CHO-E monolayers and VCAM-1, whereas very few RA+ T cells interacted with these surfaces. VCAM-1-dependent rolling was blocked completely by anti-very late Ag-4 (VLA-4) Abs. Purified CD4+RA+ T cells could be converted to RO+ cells by mitogen stimulation and 7-day culture in vitro, and this correlated with the acquisition of the ability to roll on E- or P-selectin, but not on VCAM-1 under flow. In summary, these data indicate that CD45RO+ cells interact with E- and P-selectins and VCAM-1 much more effectively than do CD45RA+ cells under flow conditions, and these adhesion pathways may contribute, either individually or in combination, to the preferential recruitment of memory T cells to peripheral sites of inflammation.
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PMID:CD45RA-RO+ (memory) but not CD45RA+RO- (naive) T cells roll efficiently on E- and P-selectin and vascular cell adhesion molecule-1 under flow. 910 26

Neurologic injury in infection with Borrelia burgdorferi can be due to the direct action of the spirochetes and spirochetal products on neural cells. There is in vitro evidence for the adherence of this organism to neurons, to glia, and to Schwann cells. Adhesion was found to be associated with galactocerebroside, a glycolipid component of myelin, and could act as a receptor for B. burgdorferi in oligodendroglia and in Schwann cells. Another pathway for neurologic injury could be through amplification of the inflammatory response by newly invading organisms (acute) and persisting (chronic) organisms. There is experimental evidence for production of IL-6, TNF-alpha, and nitric oxide by neural cells exposed to B. burgdorferi. Similar findings have been obtained from neuroborreliosis patients. Although less likely, there is the possibility that autoreactive mechanisms could have a role in the development of some manifestations of neuroborreliosis.
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PMID:Mechanisms of injury in Lyme neuroborreliosis. 916 61

Development of lymphoid progenitors in vivo requires interaction with a bone marrow stromal microenvironment containing multiple cytokines involved in the development of nonlymphoid hemopoietic lineages. We tested the effect of one such cytokine, TGF-beta, on the proliferation of early human clonogenic lymphoid progenitors using a stroma-dependent in vitro culture system. TGF-beta caused a dose-dependent inhibition of lymphoid progenitor colonies that was reversible at low TGF-beta doses by addition of exogenous IL-7 to the cultures. IL-7 was unable to reverse the inhibitory effect of higher TGF-beta concentrations or inhibition caused by IL-1alpha, IL-4, or TNF-alpha. Stromal IL-7 mRNA expression and protein secretion were markedly down-regulated by TGF-beta, suggesting that inhibition of stromal IL-7 secretion partially accounts for the inhibitory effect of TGF-beta on lymphopoiesis in this culture system. It is likely that higher TGF-beta concentrations do not inhibit lymphopoiesis by down-regulating IL-7 receptor expression, since this cytokine did not reduce IL-7R alpha or gamma c mRNA levels in normal B cell precursors. Since direct stromal contact is required for in vitro lymphopoiesis, the potential regulation of the IL-7 pathway by cell adhesion was examined. Adhesion of human B cell precursors to stroma did not alter stromal IL-7 expression or expression of IL-7R alpha or gamma c-chains by B cell precursors. These results indicate that TGF-beta is a significant negative regulator of stroma-dependent proliferation of early human lymphoid progenitors and acts in part by down-regulating stromal IL-7 secretion.
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PMID:TGF-beta down-regulates stromal IL-7 secretion and inhibits proliferation of human B cell precursors. 920 Apr 46

Adhesion mechanisms mediated by cytokines have been recognized to play a crucial role in ischaemia-reperfusion mechanisms. Although this phenomenon has been well investigated in organ transplantation, little data is available from upper extremity surgery. Profiles of adhesion molecules (CD11/CD18), key cytokines (TNF-alpha and IL-1), CD4+ and CD8+ lymphocytes, and polymorphonuclear neutrophils were investigated following controlled tourniquet ischaemia of the upper extremity for elective hand surgery. Data suggest that relatively short periods of ischaemia activate a mediator cascade and cell-cell interactions that may be associated with adverse pathopyhsiological effects on peripheral tissues after prolonged ischaemia.
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PMID:Adhesion receptors and cytokine profiles in controlled tourniquet ischaemia in the upper extremity. 945 87

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