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

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.
 ...
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

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.
 ...
PMID:Differing regulation of major histocompatibility class II and adhesion molecules on human umbilical vein endothelial cells by serotonin. 903 94

Cardiopulmonary bypass (CPB) is associated with a whole body inflammatory response which may have detrimental consequence resulting in post perfusion syndrome. Adhesion molecule E-selectin plays a pivotal role in the inflammatory response, especially in the interaction of endothelium and neutrophils. Soluble form of E-selectin (sE-selectin) is thought to be a marker of endothelial activation. To evaluate the activation of endothelium during CPB with heparin coated and un-coated extracorporeal circuits, we measured plasma levels of sE-selectin, tumor necrosis factor alpha (TNF alpha), and neutrophil elastase in 16 patients having coronary artery bypass grafting. sE-selectin plasma concentration increased during or after CPB. Significantly lower maximum levels of sE-selectin are observed in patients perfused with heparin coated extracorporeal circuits. Maximum values of sE-selectin correlated with plasma levels of TNF alpha and neutrophil elastase in each patient. These observations suggest that endothelium is activated by extracorporeal circulation in cardiac surgery, and this activation was attenuated by heparin coating of extracorporeal circuits.
 ...
PMID:[Activation of endothelium in cardiac surgery: the circulating levels of soluble E-selectin as a marker of the activation of endothelium]. 912 18

Extraintestinal dissemination of Entamoeba histolytica is frequently manifested by the life-threatening amebic liver abscess (ALA). The hepatic establishment of amebas implies invasion of blood vessels and contact with the endothelium. By means of a fluorescence-based quantitative adhesion assay, we assessed the binding to human endothelial cells of two E. histolytica strains of different virulence. The highly virulent strain (L-A) adhered substantially more strongly to unstimulated endothelium than the non-virulent one (BG3). Attachment of L-A was increased by treatment of endothelial cells with interleukin-1 beta (IL1 beta). Other proinflammatory cytokines such as interferon-gamma (IFN gamma) and tumor necrosis factor-alpha (TNF alpha) did not modify the spontaneous adhesion capacity of amebas. For purposes of comparison we also performed adhesion of the parasites to skin fibroblasts. Adhesion to this cell type was quite low (< 10%). Parasite virulence, differential adhesive capacity to endothelial cells, and modulation of the latter phenomenon by proinflammatory factors (IL1 beta) may influence the evolution and outcome of extraintestinal amebiasis, especially hepatic abscesses.
 ...
PMID:In vitro Entamoeba histolytica adhesion to human endothelium: a comparison using two strains of different virulence. 913 67

It is well known that adherence of monocytes (MO) to extracellular matrix substrates or tissue culture plastic activates these cells and induces the expression of a multitude of genes. Especially, it was described, that MO are primed by cell adhesion to produce higher amounts of some cytokines, e.g. interleukin (IL)-8 and tumor necrosis factor alpha (TNF-alpha). In order to investigate adherence-induced effects upon cytokine production, we seeded MO into tissue cultures and stimulated cells by lipopolysaccharide (LPS) simultaneously or at later time points. An increasing time-lag between cell adhesion and LPS-stimulation led to differential effects upon cytokine production: whereas TNF was upregulated (in accordance with reports by others), granulocyte colony-stimulating factor (G-CSF) was considerably down-regulated. In contrast, G-CSF production did not change, when cells were kept under non-adherent conditions in whole blood. In adherent cultures down-regulation of G-CSF could already be observed after two hours with a maximum after 24 h and was paralleled by a much lower abundance of G-CSF mRNA. Adhesion induced a significant suppression of G-CSF comparable to MO, if mature macrophages derived from MO in vitro were examined. Furthermore, two other cytokines, granulocyte-macrophage (GM)-CSF and IL-6, were also down-regulated following adhesion. In conclusion, activation of mononuclear phagocytes by adhesion can lead to "priming" for the production of some cytokines and at the same time to "silencing" for the production of others.
 ...
PMID:Differential effects of cell adherence on LPS-stimulated cytokine production by human monocytes and macrophages. 914 30

Adhesion of activated natural killer (A-NK) cells to activated and nonactivated endothelial cells in vitro was studied under dynamic flow conditions. Endothelial cells grown on glass slides were either treated with tumor necrosis factor-alpha (TNF alpha) or medium, then placed into a flow chamber over which suspensions of A-NK cells were passed using a range of defined shear stress levels. Significant numbers of binding cells could be consistently observed at shear stress levels less than 3 dyn/cm2 on TNF alpha-activated endothelium or at 0.59 dyn/cm2 on nonactivated endothelium. Stable adhesion occurred rapidly following the initial interaction of the following cells with the endothelium in the absence of detectable rolling. Pretreatment of the A-NK cells with monoclonal antibodies directed against CD18 (LFA-1) or CD49d (VLA-4) resulted in a significant reduction in the number of binding cells. Simultaneous treatment with both monoclonal antibodies eliminated all A-NK adhesion occurring over 0.5 dyn/cm2. Pretreatment of the endothelial cells with antibodies against E- or P-selectin resulted in a small but significant reduction in binding only at 0.5 dyn/cm2. The binding efficiency of the A-NK cells was similar to that previously observed for T lymphocytes under the same conditions. Once bound, approximately half of the adherent cells could resist detachment when exposed to wall shear stresses over 12 dyn/cm2. These findings indicate that A-NK cell adhesion to activated endothelium can occur under shear stress conditions which are representative of postcapillary venules and that this binding is mediated principally by both CD18 and CD49d. A-NK cell adhesion also occurs to nonactivated endothelium but only at wall shear stress levels less than 1 dyn/cm2.
 ...
PMID:Adhesion of activated natural killer cells to tumor necrosis factor-alpha-treated endothelium under physiological flow conditions. 916 65

Endothelial cell adhesion to von Willebrand Factor is mainly mediated through an interaction between the alpha vbeta3 integrin and the RGD sequence of von Willebrand factor (vWF). To define the potential involvement of glycoprotein Ib alpha (GPIb alpha) as an endothelial vWF receptor, we compared cell adhesion to three recombinant vWF, the wild-type (WT-rvWF) and two mutants, RGGS-rvWF (D1746G), defective for binding to platelet alphaIIb beta3, and deltaA1-rvWF with a deletion between amino-acids 478 and 716, which does not bind to platelet GPIb alpha. Adhesion of human umbilical vein endothelial cells to purified vWF recombinants was measured by automatized cell counting using an image analyzer. Whereas cell adhesion to delta A1-rvWF was unchanged compared with WT-rvWF, reaching a plateau of 40% total cells at a concentration of 2.5 microg/mL rvWF, adhesion to RGGS-rvWF was only 10% of total cells. Cell stimulation by tumor necrosis factor-alpha (TNF alpha), reported to upregulate the expression of the putative endothelial GPIb alpha, did not modify adhesion to these rvWF. Monoclonal antibodies to vWF or GPIb alpha, blocking vWF interaction with platelet GPIb alpha, were unable to inhibit endothelial cell adhesion to rvWF. In contrast, antibody 9 to vWF, blocking the alpha vbeta3-dependent endothelial cell adhesion to plasma vWF, inhibited adhesion to WT-rvWF as efficiently as to deltaA1-rvWF (50% inhibition at a concentration of 11 and 15 microg/mL, respectively). In agreement with the fact that endothelial cell adhesion to vWF appeared independent of the GPIb alpha-binding domain, we were unable to detect endothelial surface expression of GPIb alpha by flow cytometry or in cell lysates by immunoprecipitation followed by immunoblotting. Moreover, expression of GPIb alpha mRNA was undetectable in endothelial cells, even after stimulation by TNF alpha. These studies indicate that GPIb alpha is not expressed in human cultured endothelial cells and is not involved in adhesion to vWF-containing surfaces. Thus, in static conditions, cultured endothelial cells adhere to vWF through an alpha vbeta3-dependent, GPIb alpha-independent mechanism.
 ...
PMID:Relative importance of the glycoprotein Ib-binding domain and the RGD sequence of von Willebrand factor for its interaction with endothelial cells. 931 Apr 84

Oral ulcerations associated with HIV infection include recurrent aphthous ulcers (RAU). Whereas RAU prevalence is not increased, lesion severity is: among a group of HIV+ patients, 66% had the more severe herpetiform or major RAU. This increased severity suggests that HIV disease-related changes in the immune system may exacerbate RAU. In the peripheral blood of healthy subjects with RAU, CD4:CD8 cell ratios may be reversed and the proportion of T cell receptor-gamma delta + cells increased. HIV disease-related immune system changes are characterized by reversed CD4:CD8, lowered CD4 cell counts and an inverse correlation between CD4 cell counts and per cent activated gamma delta lymphocytes. Adhesion molecules and cytokines involved in lymphocyte homing may be important in RAU pathogenesis: ICAM-I and ELAM are strongly expressed, and TNF alpha production is increased in peripheral blood lymphocytes of healthy patients with RAU. In patients with active HIV disease/AIDS, serum TNF alpha levels are increased. Thalidomide, which inhibits TNF alpha production, is effective treatment for RAU. Some RAU patients have vitamin B12 or folate deficiencies, levels of which are commonly low in HIV+/AIDS patients. However, in a case control study of HIV+ patients, vitamin B12- or folate-deficiencies were not found to be significant risk factors for RAU.
 ...
PMID:Oral ulceration in HIV infection: investigation and pathogenesis. 945 87

Leukosialin is a negatively-charged mucin-like membrane protein of leukocytes. This anti-adhesive molecule prevents uncontrolled cellular interactions and is proteolytically cleaved during neutrophil activation. CD43 is shed in vivo during neutrophil migration to the inflammatory site. We have analysed the decrease in CD43 expression during in vitro adherence of TNF-alpha activated PMN. CD43 was quantitated by flow cytometry on TNF-alpha-activated PMN either maintained in suspension or allowed to adhere then detached with EDTA. Although TNF did not induce significant modification of CD43 expression on suspended cells, we showed that 40% of membrane CD43 is released during neutrophil TNF-induced adhesion to serum-coated plates or endothelial cells, and that migration through the endothelial monolayer did not result in further shedding. Adhesion-blocking anti-beta 2 integrin mAbs prevented CD43 shedding. beta 2 integrin "activation" by anti-CD 18 mAbs or Mn ions did not decrease CD43 expression if adhesion was prevented by stirring. Inhibitors of signal transduction or of cytoskeleton association, which allowed cells to adhere but not to spread, inhibited the shedding of CD43 during adhesion. We conclude that CD43 shedding is not promoted by beta 2 integrins engagement or adhesion but is concomitant with spreading of adherent cells.
 ...
PMID:CD43 (sialophorin, leukosialin) shedding is an initial event during neutrophil migration, which could be closely related to the spreading of adherent cells. 963 35

Adhesion molecules and cytokines are important in chronic inflammatory conditions such as rheumatoid arthritis (RA) by virtue of their role in cell activation and emigration. Using immunohistochemical techniques we studied the expression of adhesion molecules and cytokines in cryopreserved sections of murine knee joint in the course of antigen-induced arthritis, an animal model of human RA. Various adhesion molecules and cytokines are expressed in the arthritic joint tissue. LFA-1, Mac-1, CD44, ICAM-1 and P-selectin were strongly expressed in the acute phase and to a lesser degree in the chronic phase of arthritis. VLA-4 and VCAM-1 appeared to be moderately expressed on day 1, L-selectin between days 1 and 3. LFA-1, Mac-1, CD44, alpha 4-integrin, ICAM-1 and the selectins were found expressed on cells of the synovial infiltrate, LFA-1, Mac-1 and ICAM-1 on the synovial lining layer, and VCAM-1 and P-selectin on endothelial cells. Expression of E-selectin could be demonstrated throughout the experiment at a low level in cells of the acute cell infiltrate. Cytokines, especially IL-2, IL-4, IL-6, TNF, and IFN-gamma, were heavily expressed during the acute phase of arthritis in cellular infiltrate. Taken together these data demonstrate that cytokines and their activation of adhesion molecules contribute to cell infiltration and activation during the initial phase of arthritis and to the induction and progression of tissue destruction in arthritic joints. These molecules might be potential targets for novel therapeutic strategies in inflammatory and arthritic disorders.
 ...
PMID:Expression of cell adhesion molecules and cytokines in murine antigen-induced arthritis. 975 22


<< Previous 1 2 3 4 5 6 7 8 9 Next >>