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

Adhesion is a crucial requirement for the correct regulation of immune and inflammatory responses. In the immune system, leukocytes can interact with each other and with vascular endothelium as well as with extracellular matrix components, changing rapidly and transiently from circulating non-adherent to adherent states. Most of these interactions are mediated by integrins. This review will focus mainly on the structure and function of integrins expressed by leukocytes. The mechanisms for regulating the functional activity of these adhesion receptors, as well as the intracellular signals transduced through integrins, are described.
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PMID:Leukocyte integrins: structure, function and regulation of their activity. 132 Apr 33

T lymphocytes and neutrophils accumulate in psoriatic epidermis. To determine whether the epidermis plays an active role in this process through the production of cellular adhesion factors, leucocyte adherence to lesional psoriasis was compared with normal skin in a modified frozen-section adhesion assay. Lymphocyte and neutrophil suspensions were prepared by standard Ficoll-Hypaque techniques from peripheral blood of normal volunteers and overlaid on to glutaraldehyde-fixed 8-microns cryostat sections of skin. Adhesion of phorbol ester-activated T lymphocytes to the epidermis was significantly greater in psoriasis compared with normal skin (P < 0.01). Adhesion was absent (a) at 7 degrees C, (b) in the presence of EDTA and (c) in the absence of lymphocyte activation. Immunostaining demonstrated that all adherent lymphocytes were CD3+ve (i.e. T cells). Likewise, neutrophils adhered more prominently to psoriatic epidermis. Adhesion was most prominent at the tips of dermal papillae, corresponding to areas of maximal intercellular adhesion molecule-1 (ICAM-1) expression. Both neutrophils and lymphocytes adhered to dermal papillary vascular endothelium. These studies provide functional data that psoriatic epidermal cells are actively involved in leucocyte adherence. The distribution of adhesion suggests that both ICAM-1-dependent and independent mechanisms are involved.
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PMID:Preferential adherence of T lymphocytes and neutrophils to psoriatic epidermis. 135 9

Adhesion to and penetration through the sinusoidal vascular endothelium is a mandatory step for leukocyte migration and accumulation at sites of liver inflammation. This leukocyte trafficking is controlled by interactions between adhesion molecules on leukocytes and corresponding ligands on endothelial cells. We have analyzed the in situ distribution of two recently described vascular adhesion molecules (i.e., endothelial leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1) and of the lymphocyte "homing" receptor cluster of differentiation antigen-44 in normal and inflamed liver biopsy specimens. Endothelial leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1 were absent from normal liver tissue, but they were strongly expressed on sinusoidal lining cells in inflammatory liver disease. Endothelial leukocyte adhesion molecule-1 expression predominated diffusely throughout the liver parenchyma in acute hepatitis; in contrast, vascular cell adhesion molecule-1 was mainly expressed in areas of periportal and intralobular inflammation in chronic active and persistent hepatitis. The "homing" receptor cluster of differentiation antigen-44 was weakly expressed on scattered mononuclear cells and on sinusoidal lining cells in normal liver tissue, but it was strongly up-regulated on mononuclear inflammatory cells and sinusoidal lining cells in acute and chronic hepatitis. In addition, reactivity for the cluster of differentiation antigen-44 was found on the membranes of variously sized clusters of hepatocytes in biopsy specimens with acute hepatitis. De novo or up-regulated expression of these adhesion molecules on sinusoidal lining cells in inflamed liver biopsy specimens indicates that these cells actively modulate their phenotype in response to environmental factors, thus playing a key role in the recruitment of leukocytes in acute and chronic liver inflammation.
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PMID:Vascular adhesion molecules in acute and chronic liver inflammation. 137 Sep 47

The adhesion of circulating leukocytes to the vascular endothelium is essential for effective host inflammatory and immune responses. Adhesion proteins expressed by both the leukocyte and endothelial cell have been well characterized, and studies of these molecules have shown that both cell types are actively involved in regulating these binding events. Most leukocyte (leukocyte integrins) and endothelial cell (vascular selectins, ICAM-1, and VCAM) adhesion proteins increase in expression and function in response to mediators released by inflamed tissues. In contrast, the expression and function of one type of leukocyte molecule, L-selectin (previously called LECAM-1, LAM-1, gp90MEL-14), is "down-regulated" by inflammatory signals. The purpose of this review is to summarize in vitro and in vivo regulatory and functional studies of some of the molecular mechanisms which regulate leukocyte-endothelial cell adhesion, with particular emphasis on L-selectin, and to present a hypothetical model of how these molecules may be orchestrated in vivo resulting in the control of host inflammatory responses.
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PMID:Leukocyte traffic to sites of inflammation. 137 85

Adhesion of leukocytes to vascular endothelium is a necessary step leading to the migration of cells into underlying tissues. Vascular adhesion molecules regulate this process and may play an important role in graft rejection. Immunocytochemical studies have been used to investigate the expression of vascular adhesion molecules (ICAM-1, PECAM, VCAM-1, and ELAM-1) in normal donor heart (n = 15) and myocardial biopsies from heart transplant patients with acute rejection (n = 15). Sections were also stained with antibodies against endothelium, leukocytes, MHC antigens, and markers of cell activation. In donor heart EN4, vWF, ICAM-1, PECAM, MHC class I--and, to a lesser extent, VCAM-1 and DR antigen--are expressed on arterioles and venules, whereas ELAM-1 and Pal-E are restricted to venules. Expression of Pal-E, VCAM-1, ICAM-1, and DR antigen was increased during rejection. Capillary endothelium normally expresses EN4, ICAM-1, PECAM, MHC class I, and DR antigen but little, if any, VCAM-1 or ELAM-1. During rejection, however, there is an increased expression of all adhesion molecules. This is paralleled by an increased expression of vWF by capillary endothelium. In addition, ICAM-1 like MHC class I antigen is induced on the myocardial membrane and intercalating discs. Endocardium from donor heart expresses EN4, vWF, PECAM, MHC class I, and sometimes Pal-E and ICAM-1, but very little VCAM-1, ELAM-1 or DR antigen. There is an increased expression of Pal-E, ICAM-1, VCAM-1, and DR antigen on endocardium from rejecting heart biopsies. Proliferating Ki-67+ cells and activated T cells expressing the receptor for IL-2 were also found in biopsies during rejection episodes.
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PMID:Induction of vascular adhesion molecules during rejection of human cardiac allografts. 138 80

Adhesion of polymorphonuclear leukocytes (PMN) to vascular endothelium is one of the first events in their response against local bacterial infection. Different adhesion molecules sequentially mediate PMN adherence to endothelium and extravasation into inflamed tissues. We show that bacterial extracts OM-85 BV and OM-89 increase the expression of adhesion molecules at the surface of PMN and we suggest that this upregulation could be linked to the beneficial effect of bacterial extracts in the prevention of respiratory tract infections.
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PMID:Adhesion molecules in antibacterial defenses: effects of bacterial extracts. 143 36

1. Vascular injury during the intra-operative procedures of bypass surgery may be the initiating event in the gradual deterioration in the patency of the graft. Adhesion of leukocytes to the vascular endothelium frequently accompanies preparation and insertion of the graft. However, little is known about the effects of vasoactive substances released from leukocytes on vein graft performance. 2. To determine whether leukotrienes are capable of affecting the tone of blood vessels used as coronary artery bypass grafts we studied the human saphenous vein as intact rings using an isolated organ bath technique. 3. LTC4 and LTD4 caused weak endothelium-dependent relaxations at lower concentrations (1 pM to 1 nM) and powerful endothelium-independent contractions at higher concentrations (3 nM to 0.1 microM). The maximum responses to LTC4 and LTD4 for relaxations were 21.1 +/- 4.8% and 28.6 +/- 3.4% (% of noradrenaline induced tone) respectively and 64.6 +/- 9.9% and 59.1 +/- 7.9% (% response to KCl) respectively for contractions. 4. The inhibitor of nitric oxide formation, L-NG-monomethyl L-arginine, prevented the relaxations to LTD4, but not LTC4 and unmasked endothelium-dependent contractions to LTD4 (32.9 +/- 11.3%). NG-monomethyl L-arginine had no effect on the contractions produced by LTC4 or LTD4. 5. Indomethacin augmented relaxations and contractions of saphenous vein to LTC4 from 22.5 +/- 5.6 to 40.02 +/- 8.7 (P < 0.05) and 48.8 +/- 5.5% to 74.7 +/- 7.6% (P < 0.01) respectively. LTD4 responses were not affected by indomethacin treatment. 6. In conclusion, leukotrienes mediate biphasic responses in the human saphenous vein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of leukotrienes C4 and D4 on human isolated saphenous veins. 146 35

Lipoprotein lipase (LPL) bound to vascular endothelial cells hydrolyses triglycerides in plasma lipoproteins. To explore the role of LPL in atherogenesis, the effect of LPL-mediated lipolysis of very low density lipoproteins (VLDL) on monocyte adhesion to endothelial cells was examined. Adhesion of U937 monocytes to porcine aortic endothelial cells that were incubated with VLDL and purified bovine milk LPL was markedly higher than endothelial cells that were incubated with VLDL alone. The increase in monocyte adhesion obtained with VLDL was dependent on the concentration of the lipoprotein, monocyte dose and time of incubation. The increase in adhesion correlated with generation of free fatty acids from the hydrolysis of triglycerides in VLDL by LPL. Furthermore, direct addition of oleic acid to endothelial cells also increased adhesion of monocytes. We postulate that LPL-derived lipolytic products increase monocyte adhesion to vascular endothelium and thereby promote atherogenesis.
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PMID:Lipoprotein lipase-mediated lipolysis of very low density lipoproteins increases monocyte adhesion to aortic endothelial cells. 148 70

The regulation of lymphocyte migration to specific tissues is complex and involves lymphocyte-endothelial interactions at sites of extravasation. Adhesion molecules play a vital role in the migration of lymphocyte into and out of the tissues. Therefore, excessive induction of adhesion molecules on the vascular endothelium might result in the accumulation of lymphocytes in the rheumatoid synovium. The rheumatoid synovium exhibits functionally as well as morphologically altered synovial vessels, which are probably induced by inflammatory mediators. It should be pointed out that the immunocompetent cells confront various extracellular matrix after extravasation. The signalling through receptors for extracellular matrix modify the subsequent cellular responses against certain target tissues. Thus, interaction of immunocompetent cells with endothelium as well as extracellular matrix through adhesion molecules is critical for the pathogenesis of rheumatoid arthritis.
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PMID:[Aberrant expression of adhesion molecules in rheumatoid arthritis]. 158 30

Adhesion of circulating leukocytes to the vascular endothelium during inflammation is mediated in part by their interaction with the endothelial-leukocyte adhesion molecule ELAM-1. ELAM-1, a member of the LEC-CAM family of cell adhesion molecules, expresses an N-terminal carbohydrate recognition domain (CRD) homologous to various calcium-dependent mammalian lectins. However, the contribution of the CRD to cell adhesion and its carbohydrate binding specificity have not been elucidated. This study demonstrates that transfection of a human fucosyltransferase cDNA into nonmyeloid cell lines confers ELAM-1--dependent endothelial adhesion. Binding activity correlates with de novo cell surface expression of the sialylated Lewis x tetrasaccharide, whose biosynthesis is determined by the transfected fucosyltransferase cDNA. We propose that specific alpha(1,3)fucosyltransferases regulate cell adhesion to ELAM-1 by modulating cell surface expression of one or more alpha(2,3)sialylated, alpha(1,3)fucosylated lactosaminoglycans represented by the sialyl Lewis x carbohydrate determinant.
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PMID:ELAM-1--dependent cell adhesion to vascular endothelium determined by a transfected human fucosyltransferase cDNA. 169 67


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