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

Adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and its counter-receptor, lymphocyte function associated antigen-1 (LFA-1), play very important roles in immune responses. In this study, the effects of cytokines on cultured human melanoma cells (MMG2) were examined, especially focussing on the expression of ICAM-1 on MMG2 and lymphocyte adhesion to MMG2. Both the expression of ICAM-1 and HLA-DR on MMG2 increased after treatment with IFN-gamma. ICAM-1 expression began to increase earlier than HLA-DR expression. TNF-alpha and IL-1 beta also increased the expression of ICAM-1 on MMG2. However, these cytokines did not increase the expression of HLA-DR. IFN-gamma had a dose dependent effect on lymphocyte adhesion to MMG2. Pretreatment of IFN-gamma treated MMG2 with 84H10 (anti-ICAM-1 antibody) or pretreatment of lymphocytes with either SPV-L7 (anti-LFA-1 alpha antibody) or IOT10 (anti-LFA-1 beta antibody) inhibited the lymphocyte adhesion to MMG2. These results suggest that ICAM-1 molecules induced on melanoma cells by IFN-gamma can interact with LFA-1 molecules on lymphocytes.
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PMID:Intercellular adhesion molecule-1 on cultured human melanoma cells: influence of cytokines. 809 20

Clinically, there is an association between CMV infections and the occurrence of rejection after renal transplantation. Adhesion molecules such as intercellular adhesion molecules (ICAM) and MHC Ags are thought to be important in the induction and amplification of the rejection process. Therefore, we studied ICAM-1 and MHC expression after CMV infection or stimulation with cytokines. Cultured proximal tubular epithelial cells (PTEC) were stimulated with cytokines or infected with CMV. MHC class I, class II, and ICAM-1 expression were determined by radioimmunoassay. IFN-gamma induced class II and ICAM-1 expression. Small concentrations of IFN-alpha inhibited the IFN-gamma induced class II expression. CMV-infected PTEC displayed increased levels of ICAM-1 and class I expression. This enhancement is a direct effect of the virus on the infected cells and not mediated by soluble factors. Although MHC class II expression is not directly enhanced by CMV, infected PTEC display a normal increase of class II expression after stimulation with IFN-gamma.
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PMID:Cytomegalovirus directly enhances MHC class I and intercellular adhesion molecule-1 expression on cultured proximal tubular epithelial cells. 810 91

We determined the ability of proinflammatory cytokines to enhance ICAM-1 (CD54) expression on, and PBMC adhesion to, human synoviocytes. Surface molecules were characterized by cell ELISA and by flow cytometry. Adhesion of PBMC to synoviocyte monolayers was measured by direct counting or by colorimetric staining. Most cytokines upregulated ICAM-1 expression (IL-1 beta > TNF alpha > IFN-gamma >> PDGF-bb, IL-6), but not GM-CSF or TGF beta. A similar concentration-dependent increase was observed for synoviocytes derived from patients with rheumatoid or osteoarthritis. Kinetic studies of ICAM-1 expression differed among several cytokines: an early rise with IL-1 beta or TNF alpha stimulation, a gradual increase with IFN-gamma, a transient increase with PDGF-bb, and a plateau with IL-6. Adhesion of PBMC to synoviocytes was increased by IL-1 beta or TNF alpha and reduced by MAb to CD54 or CD18. Increased synoviocyte adhesiveness may promote interactions with infiltrating inflammatory cells.
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PMID:Proinflammatory cytokines enhance human synoviocyte expression of functional intercellular adhesion molecule-1 (ICAM-1). 810 22

Microvascular endothelial cells derived from the blood-retinal barrier were grown in vitro and various factors affecting the adhesion of syngeneic lymphocytes to these monolayers was evaluated. Under resting conditions 5.3 +/- 0.4% of lymphocytes derived from peripheral lymph nodes (PLN) were found to adhere to the endothelia. Adhesion of resting lymphocytes increased significantly following endothelial treatment with interferon-gamma (IFN-gamma; 11.7 +/- 1.0%), interleukin-1 (IL-1; 14.9 +/- 1.2%), astrocyte conditioned medium (ACM; 12.7 +/- 0.9%) or forskolin (13.9 +/- 1.2%). Lymphocyte activation with concanavalin A (ConA) increased adhesion to 17.0 +/- 0.9% which could be augmented by activating the endothelia with IFN-gamma (22.3 +/- 1.0%), IL-1 (24.0 +/- 1.0%) and ACM (25.7 +/- 1.6%). An antigen-specific CD4+ T cell line exhibited the greatest degree of adhesion, 40.4 +/- 2.5% on resting endothelia, 60.0 +/- 3.0% on IFN-gamma-activated cells and 54.3 +/- 1.4% on IL-1-activated cells. Although CD4+ lymphocytes predominated in the PLN population by 2:1, significantly more CD8+ cells were found to adhere.
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PMID:Lymphocyte adhesion to cultured endothelial cells of the blood-retinal barrier. 822 14

Monocyte migration within the extravascular space of inflamed tissues is controlled by adhesion molecules and inflammatory cytokines. In this study, we analyzed the capacity of TGF-beta 1 and IFN-gamma to regulate adhesion of human activated monocytes to fibronectin (FN) and to laminin (LM), two components of the extracellular matrix. When cultured in the absence of any of these two stimuli, human monocytes underwent "spontaneous activation" and adhered to both FN and LM. Adhesion to FN was inhibited in the presence of alpha 5 and beta 1 integrin blocking antibodies, whereas beta 2 blocking antibody blocked attachment to LM. Exogenous TGF-beta 1 increased the adhesive ability of monocytes to FN and to LM, respectively, linked to the increase of alpha 5 and beta 2 mRNA and protein synthesis levels. Moreover, an increase in alpha 5 expression at the monocyte cell surface was observed. In contrast, monocytes stimulated with exogenous IFN-gamma lost their capacity to bind to FN and this coincided with the down-regulation of surface alpha 5 expression which occurred at the posttranscriptional level of alpha 5 synthesis. Although IFN-gamma-treated monocytes also showed a decreased ability to adhere to LM, no alteration of beta 2 mRNA levels, beta 2 protein synthesis, and beta 2 cell surface expression was detectable, thus suggesting a modification of the functional state of surface beta 2 integrins. Furthermore, when stimulated with TGF-beta 1, IFN-gamma-pretreated monocytes reacquired the ability to bind to FN and LM. Conversely, IFN-gamma reduced adhesiveness to FN and LM of monocytes initially stimulated with TGF-beta 1. These in vitro adhesive-deadhesive responses of monocytes to TGF-beta 1 and IFN-gamma modulation may reflect mononuclear phagocyte motility within sites of inflammation.
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PMID:TGF-beta 1-stimulated adhesion of human mononuclear phagocytes to fibronectin and laminin is abolished by IFN-gamma: dependence on alpha 5 beta 1 and beta 2 integrins. 854 65

Adhesion molecules and cytokines are involved in regulation of cellular host responses in infection processes. In this study the roles of the integrins Mac-1 and VLA-4, as well as those of the cytokines tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma), in defense mechanisms against Yersinia enterocolitica in Peyer's patches (PP) and mesenteric lymph nodes (MLN) were investigated by blocking these molecules with antibodies in vivo prior to orogastric Yersinia infection. Intestinal Yersinia infection caused abscesses composed of polymorphonuclear (Mac-1+ VLA-4+ Pgp-1+ ICAM-1-) and mononuclear (Mac-1+ VLA-4+ Pgp-1+ ICAM-inhibited phagocytosis of yersiniae by macrophages, (ii) reduced Yersinia-specific proliferation and IFN-gamma production of T cells from PP and MLN, and (iii) caused increased bacterial growth in PP and MLN followed by profound tissue destruction. Neutralization of TNF-alpha or IFN-gamma had comparable effects, suggesting that cell-mediated host responses including activated macrophages are required for control of yersiniae in intestinal tissues. The number of Mac-1+ cells in PP and MLN increased after yersinia infection, and recruitment of these cells was not blocked by administration of anticytokine or anti-integrin antibodies. While anti-VLA-4, -TNF-alpha, or -IFN-gamma antibody treatment caused an increased dissemination of yersiniae from PP to the spleen systemic dissemination was reduced by anti-Mac-1 antibodies. The results of this study suggest that the cytokines IFN-gamma and TNF-alpha as well as the integrins Mac-1 and VLA-4 are involved in protective cellular host defense mechanisms in PP and MLN against Y. enterocolitica, the latter probably being involved in both cell-cell and cell-pathogen interactions.
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PMID:Defense mechanisms in Peyer's patches and mesenteric lymph nodes against Yersinia enterocolitica involve integrins and cytokines. 860 1

Endothelial cell (EC) junctions regulate circulating leukocyte extravasation and infiltration at inflammatory sites. Several lines of evidence show that platelet endothelial cell adhesion molecule-1 (PECAM-1), a specific component of EC junctions, is required for leukocyte transmigration through EC monolayers. In this paper, we examined the effects of two inflammatory cytokines, TNF-alpha and IFN-gamma, on PECAM-1 and vascular endothelial-cadherin/catenin organization. We found that the addition of inflammatory cytokines (TNF-alpha plus IFN-gamma in combination, for > or = 24 h) caused PECAM-1 to disappear from EC intercellular contacts. Confocal microscopy indicated that after treatment with the cytokines, PECAM-1 was rapidly internalized. In addition, a strong inhibition of PECAM-1 synthesis and a decrease in PECAM-1 mRNA were observed. This phenomenon was only found when TNF-alpha plus IFN-gamma were used in combination. Adhesion of polymorphonuclear cells to doubly treated EC was increased compared with control cells or cells incubated with TNF-alpha or IFN-gamma separately. This was correlated with an increased expression of intercellular adhesion molecule-1. However, the disappearance of PECAM-1 from cell junctions after treatment with TNF-alpha plus IFN-gamma was accompanied by a marked reduction of leukocyte migration through EC monolayers. The correlation between PECAM-1 level and leukocyte transmigration was supported by transmigration inhibition assays using blocking anti-PECAM-1 mAb. These data indicate that PECAM-1 is a specific target of inflammatory cytokines and suggest that changes in its synthesis and organization might negatively modulate leukocyte recruitment.
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PMID:Inhibition of platelet endothelial cell adhesion molecule-1 synthesis and leukocyte transmigration in endothelial cells by the combined action of TNF-alpha and IFN-gamma. 875 31

Adhesion molecules have been demonstrated immunohistochemically on smooth muscle cells in atherosclerotic plaques. In endothelial cells cytokines are potent modulators of adhesion molecule expression. We therefore investigated the effects of cytokines on adhesion molecule expression on cultured human coronary and pulmonary smooth muscle cells by cell ELISA and confocal microscopy. Human coronary and pulmonary smooth muscle cells expressed ICAM-1 and VCAM-1 but not E-selectin. ICAM-1 expression was upregulated by TNF alpha, Il-1 beta and IFN-gamma. VCAM-1 expression was increased by TNF alpha and weakly by Il-1 beta, IFN-gamma had no effect on VCAM-1 expression. Cytokine effects on ICAM-1 and VCAM-1 were based on de novo synthesis. These results demonstrate that cytokines regulate ICAM-1 and VCAM-1 expression on human coronary and pulmonary smooth muscle cells. These effects may play an important role in the immune mechanisms in atherosclerosis.
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PMID:Modulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on human coronary smooth muscle cells by cytokines. 882 78

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

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


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