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

Adhesion of lymphocytes to mouse brain endothelial cells was studied after treatment of the endothelium with 1000 U/ml gamma interferon (IFN-gamma) for 1 h to 2 days. Adhesion was not significantly different from controls after 1 h but at 4 h and thereafter, adhesion increased in a time-related manner. IFN-gamma also increased the expression of class II major histocompatibility complex (MHC) and murine intercellular adhesion molecule-1 (ICAM-1) molecules on the endothelial cells. The level of expression of class II MHC molecules was related to the length of exposure to IFN-gamma. MAb blocking studies suggested that class II molecules were responsible for the IFN-gamma-induced increase in lymphocyte-endothelial cell adhesion. Transfection of a murine lung endothelial cell line with cDNA for the class II MHC molecule also produced a significant increase in lymphocyte-endothelial cell adhesion, suggesting that the class II MHC molecule may have a role in adhesion which is distinct from antigen presentation.
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PMID:Modulation of adhesion of lymphocytes to murine brain endothelial cells in vitro: relation to class II major histocompatibility complex expression. 134 74

Monocytes and endothelial cell interactions play a key role in the development of vascular lesion, inflammation and atherosclerosis. Leukocyte adhesion is mediated through specific molecules CD11/CD18 complexes on the leukocyte side and the ELAM (Leukocyte Adhesion Molecule) ICAM (Intercellular Adhesion Molecule) on the endothelium cell surface. Several monocyte products damage endothelial cells such as free radicals, oxygen peroxides, proteases, hydrolases, lipases... Various monokines alter endothelial cell function and proliferation. Interleukin 1, gamma interferon, alpha tumor necrosis factor increase ELAM, further more they induce the synthesis of procoagulant activity by endothelial cells. Monocyte derived growth factor stimulates endothelial cells proliferation while transforming growth factors, beta (TGF beta) and TNF alpha inhibit endothelial cell growth. Lipid products of monocyte origins such as leukotrienes induce an activation of endothelial cells which results in a production of prostacyclin. Monocytes may also participate in the coagulation process by producing thromboplastin and coagulation factors and facilitating the tenase (activation of factor X) complex formation. On the other hand, monocyte also synthesize tissue plasminogen activator and inhibitor. The numerous factor produced by monocytes may affect in different ways the endothelial cell behavior.
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PMID:[Monocyte-endothelium relations]. 265 10

The present study was designed to examine the effect of Pseudomonas aeruginosa alkaline protease (AP) and elastase (Ela) on human natural killer (NK) cell activity in vitro. AP and Ela were found to inhibit NK cell function. Addition of alpha interferon and interleukin-2 did not abolish this inhibition of NK cell activity. Adhesion of effector to target cells was studied in a single-cell agarose assay of monocyte-depleted NK-cell-enriched cell populations. AP and Ela were shown to inhibit effector/target cell conjugate formation. Furthermore, AP and Ela inhibited the binding of the monoclonal antibody Leu-11, which reacts with the Fc receptor of NK cells. The inhibition of NK cell binding to the target cell by P. aeruginosa proteases is most likely due to proteolytic cleavage of the surface receptors involved in the binding of the effector cell to the target cell.
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PMID:Inhibition of human natural killer cell activity by Pseudomonas aeruginosa alkaline protease and elastase. 303 Sep 37

Adhesion of lymphocytes to vascular endothelium is thought to be of importance in regulating the passage of lymphocytes from the circulation to areas of inflammation. Evidence suggests the presence of site-specific lymphocyte receptor molecules on the endothelial cell surface which can be modulated by soluble immune factors. The factors responsible for maintaining lymphocyte infiltration at tissue sites are unknown. We have examined the adherence of human peripheral blood T lymphocytes to human fibroblast monolayers in vitro and the role of interferon-gamma in enhancing adherence. Treatment of fibroblasts with interferon-gamma resulted in an increase in the number of adherent T cells in a dose- and time-dependent manner. Enhanced adhesion was noted as early as 4 hr after interferon stimulation (291 +/- 7 T cells/field vs 51 +/- 10 without IFN stimulation) and binding was further increased by lengthening the exposure time of fibroblasts to interferon up to 72 hr (475 +/- 86 T cells/field). Kinetic and inhibition experiments using monoclonal antibody to HLA-DR demonstrated that adhesion of T lymphocytes to interferon-stimulated fibroblasts proceeds by a mechanism independent of DR induction. In addition, adherence was not histocompatibility antigen-restricted, as adherence to autologous and allogeneic fibroblast monolayers was not significantly different. Nonadherent T cells, collected at the end of adhesion assays, were deficient in their capacity to bind to a second interferon-treated monolayer, suggesting the depletion of a subpopulation of T cells responsible for adhesion. Alterations of fibroblasts in vivo by immune cell-derived cytokines may be an important mechanism for the localization of lymphocytes at sites of connective tissue inflammation.
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PMID:Lymphocyte-fibroblast adhesion induced by interferon-gamma. 313 Oct 21

By using a chromogenic substrate for an ubiquitous lysosomal enzyme, hexosaminidase to estimate cell numbers, a sensitive and simple procedure has been developed in which microtiter reaction wells are directly scanned in a spectrophotometer. This method has been adapted to several cell biological assays. Quantitation of the biological activities of T cell growth factor and interferon can be performed on large numbers of samples. Adhesion of dispersed solid tissue cells to fibronectin coated substrates may be quantitated with little expenditure of reagents. By use of a panning procedure in microtiter plates a sensitive and very simple assay for the binding of monoclonal antibodies to cell surface antigens has been developed.
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PMID:Measurement of cell numbers by means of the endogenous enzyme hexosaminidase. Applications to detection of lymphokines and cell surface antigens. 620 May 37

Monocytes but not unstimulated lymphocytes adhered to human neurons and astrocytes in primary culture, as demonstrated by double labeling. The expression of VCAM-1 was higher on neurons than on astrocytes, whereas that of beta 1, alpha 1, alpha 2, alpha 4 and alpha 5 chains from the integrins and of ICAM-1 was identical on both types of cells. The expression on neurons of ICAM-1, but not of integrins, was up-regulated by exogenous tumor necrosis factor (TNF) alpha, interleukin (IL)-1 alpha and interferon (IFN)-gamma. The same was observed on astrocytes associated with a sharp increase in the expression of VCAM-1. Adhesion between monocytes and neurons or astrocytes was 80% inhibited by mAbs directed against the CR3 determinant on monocytes or against ICAM-1 on neural cells but not by any of the other mAbs against adhesion proteins that were tested. Finally, the level of endogenous production of IL-1 alpha and TNF alpha was greatly increased after the adhesion of monocytes to CNS cells.
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PMID:Adhesion to human neurons and astrocytes of monocytes: the role of interaction of CR3 and ICAM-1 and modulation by cytokines. 770 27

Adhesive interactions between murine cerebrovascular endothelial cells (EC) which comprise the blood-brain barrier (BBB) and myelin basic protein (MBP)-specific encephalitogenic T lymphocytes were investigated. Adhesion was assessed by measuring the percent attachment of 51Cr-labeled T cells to EC monolayers. The basal level adhesion (20-35%) was significantly up-regulated by treating EC with recombinant murine gamma interferon (IFN-gamma), interleukin-1 alpha (IL-1 alpha) and/or tumor necrosis factor-alpha (TNF alpha). The ability of these cytokines to modulate adhesion was dose- and time-dependent and could be detected as early as 1 h after treatment. The expression of intercellular adhesion molecule-1 (ICAM-1) by EC was examined by immunofluorescence staining and ELISA. Although all unstimulated EC cultures expressed ICAM-1, treatment of EC with the above cytokines dramatically up-regulated the level of ICAM-1 expression in a dose- and time-dependent fashion similar to that observed in the adhesion assays. Treatment of EC with transforming growth factor-beta 1 (TGF beta) down-regulated the level of T cell adhesion on untreated EC in a dose-dependent manner. Pretreatment of EC with TGF beta also partially inhibited the up-regulation of adhesion induced by IFN-gamma, IL-1 alpha and/or TNF alpha. TGF beta had no effect on the up-regulation of ICAM-1 expression induced by IFN-gamma, IL-1 alpha and/or TNF alpha. These results indicate that in addition to ICAM-1, other molecules may be involved in adhesion of encephalitogenic T cells to the EC comprising the cerebral vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokine-regulated adhesion between encephalitogenic T lymphocytes and cerebrovascular endothelial cells. 809 22

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

In our previous study, we have shown that polyinosinic-polycytidylic acid (poly I:C), a double-stranded RNA, and a potent inducer of interferon, enhanced the wound healing in rats and mice. Increased levels of laminin and collagen, and greater influx of dermal fibroblasts were observed in poly I:C-treated wounds as compared to untreated wounds (Bhartiya et al., 1992, J. Cell. Physiol., 150:312-319). In this study, we have explored the mechanism of enhanced wound healing by poly I:C in rats. Poly I:C (1 mg/kg) in phosphate buffered saline was injected intraperitoneally 18 h prior to wound healing, and the animals were sacrificed on day 3 postwounding. Immunofluorescence studies showed increased expression of adhesion molecules that includes ICAM-1 (intercellular adhesion molecule-1;CD54) and VCAM-1 (vascular cell adhesion molecule; CD 106) in poly I:C-treated wounds as compared to untreated control. Poly I:C treatment resulted in an increase in the mRNA levels of collagen type 1 (alpha), collagen III, laminin B1, and transforming growth factor-beta 1(TGF-beta 1) in wounds compared to untreated wounds as demonstrated by in situ hybridization and PCR analysis. These studies suggests that poly I:C upregulates the biosynthesis of adhesion molecules, extracellular matrix proteins (ECM), and TGF-beta 1 in the wound bed. Adhesion molecules and ECM play a major role in wound healing, and TGF-beta 1 has been known to be a potent wound healer. Therefore, the increased expression of these molecules may play a role in the enhanced healing by poly I:C observed in rats.
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PMID:Enhanced biosynthesis of extracellular matrix proteins and TGF-beta 1 by polyinosinic-polycytidylic acid during cutaneous wound healing in vivo. 884 27

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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