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

Adhesion of leukocytes to endothelial cells is a critical step in the development of acute and chronic inflammatory lesions. We report here that estradiol treatment of cultured human umbilical vein endothelial cells stimulated up to a twofold increase in TNF-induced adhesion of both polymorphonuclear leukocytes and PMA-activated peripheral blood mononuclear cells. This effect was more evident (threefold increase) when endothelial cells were cultured on the basement membrane glycoprotein laminin. Progesterone, but not testosterone, had a similar stimulatory effect. Estradiol also promoted a slight increase in interferon gamma-stimulated endothelial cell adherence for peripheral blood mononuclear cells, but no effect of estradiol was observed when adhesion of leukocytes to endothelial cells was stimulated with IL-1 or IL-4. The estradiol-induced increase in leukocyte binding to human umbilical vein endothelial cells was partially blocked by antibodies to the adhesion molecules E-selectin, intercellular adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule type 1 (VCAM-1). Indirect immunofluorescence techniques showed that estradiol produces an increase in TNF-induced cell surface expression of these molecules. Northern blot analysis demonstrated a transient increase in TNF-induced expression of mRNA for E-selectin, ICAM-1, and VCAM-1 in endothelial cells treated with estradiol. Our data demonstrate that estradiol has important regulatory functions in promoting leukocyte-endothelial cell interactions that might contribute to the observed predominance in females of some autoimmune inflammatory diseases.
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PMID:Estradiol enhances leukocyte binding to tumor necrosis factor (TNF)-stimulated endothelial cells via an increase in TNF-induced adhesion molecules E-selectin, intercellular adhesion molecule type 1, and vascular cell adhesion molecule type 1. 750 11

As in other organs, leukocyte adhesion molecules and their ligands play a major role in cutaneous inflammatory events both by directing leukocyte trafficking and by their effects on antigen presentation. Skin biopsies of inflamed skin from patients with diseases such as as psoriasis or atopic dermatitis reveal up-regulation of endothelial cell expression of P- and E-selectin, vascular cell adhesion molecule 1 and intercellular adhesion molecule 1. Studies of evolving lesions following UVB irradiation, Mantoux reaction or application of contact allergen, demonstrate that expression of these adhesion molecules parallels leukocyte infiltration into skin. When cutaneous inflammation is widespread (e.g. in erythroderma), soluble forms of these molecules are detectable in serum. In vitro studies predict that peptide mediators are important regulatory factors for endothelial adhesion molecules. Intradermal injection of the cytokines interleukin 1, tumour necrosis factor alpha and interferon gamma into normal human skin leads to induction of endothelial adhesion molecules with concomitant infiltration of leukocytes. In addition, neuropeptides rapidly induce P-selectin translocation to the cell membrane and expression of E-selectin. Adhesion molecules also play a crucial role as accessory molecules in the presentation of antigen to T lymphocytes by Langerhans' cells. Expression of selectin ligands by Langerhans' cells is up-regulated by various inflammatory stimuli, suggesting that adhesion molecules may be important in Langerhans' cell migration. The skin, because of its accessibility, is an ideal organ in which to study expression of adhesion molecules and their relationship to inflammatory events. Inflammatory skin diseases are common and inhibition of lymphocyte accumulation in skin is likely to prove of great therapeutic benefit.
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PMID:Adhesion molecules in cutaneous inflammation. 758 40

Crypt abscesses allow prolonged apposition of activated neutrophils to the epithelial surface of the colon. Adhesion of neutrophils to both the vascular endothelium and basolateral epithelial membrane share common effector molecules but are distinct processes. This study aimed to define the mechanisms that effect adhesion, independent of transmigration, to the apical epithelium. HT29 (cl 19A) cells were grown to confluency and incubated with neutrophils under conditions of: (i) neutrophil stimulation with phorbol-myristate-acetate; (ii) monolayer stimulation with interferon gamma, tumour necrosis factor alpha (IFN gamma, TNF alpha); and (iii) recent epithelial cell trypsinisation. These experiments were carried out in the presence of neutralising antibodies to CD18, CD11b, LFA-1, E-selectin, P-selectin, intracellular adhesion molecule 1 (ICAM-1), and ICAM-2; a novel CD11b/CD18 antagonist, neutrophil inhibitory factor (rNIF); adenosine receptor agonists (5'N-ethycarboxamido adenosine/N6-cylopentyladenosine (NECA/CPA)) and a platelet activating factor (PAF) receptor antagonist lexipafant. Adhesion of stimulated neutrophils to resting monolayers was Mac-1, CD18 dependent and ICAM-1, ICAM-2, E-selectin, P-selectin, PAF independent. Cytokine activated monolayers exhibited higher binding of neutrophils which was inhibited by rNIF and aCD18. Recently trypsinised monolayers bound neutrophils in a CD11b/CD18 and CD18 independent manner. Adenosine agonists failed to influence neutrophil adhesion under any condition. This study shows neutrophil adhesion to apical epithelial membranes is similar to that at the epithelial basolateral membrane, though different to that seen at the vascular endothelium. These results highlight regional differences in neutrophil adhesion molecule usage.
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PMID:Mechanisms underlying neutrophil adhesion to apical epithelial membranes. 880 Nov 97

The initiation of cytotoxic immune responses requires the direct interaction between naive CD8+ T lymphocytes and dendritic cells (DCs). Multiphoton imaging in intact lymph nodes (LNs) showed that during priming, naive T cells and DCs establish sequentially brief (i.e., minutes) and long (hours) antigen-specific contacts. We show here that the expression of the Intercellular Adhesion Molecule-1 (ICAM-1) by mature DCs is critical for long-lasting contacts with CD8+ T cells but dispensable for short-lived antigen-specific interactions. Serial brief DC-T cell contacts induced early CD8+ T cell activation, proliferation, and differentiation into effector cytotoxic T lymphocytes in the first few days after immunization. ICAM-1-deficient mature DCs, however, failed to induce fully effective priming, because CD8+ T cells produced reduced amounts of interferon gamma and were clonally depleted after 2 weeks. In addition, Icam1(-/-) mice failed to respond to rechallenge. We conclude that ICAM-1-dependent long-lasting interactions between mature DCs and naive CD8+ T cells determine the survival of activated CD8+ T cells and the establishment of effective memory.
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PMID:Intercellular adhesion molecule-1-dependent stable interactions between T cells and dendritic cells determine CD8+ T cell memory. 1827 26

Insights into sequential leukocyte-endothelial interactions during leukocyte trafficking have been obtained through experiments using human umbilical vein endothelial cells (HUVEC) under flow conditions. To investigate leukocyte-brain endothelial cell interactions, we developed a dynamic in vitro system, using Transfected Human Brain Microvascular Endothelial Cells (THBMEC) and a parallel plate flow chamber. Human peripheral blood mononuclear cells (PBMC) were perfused across confluent THBMEC cultures at a velocity that approximates the rate found in human brain capillaries. Leukocyte-THBMEC interactions were visualized by phase-contrast microscopy, and images were captured on a CCD camera. To simulate inflammatory conditions, we activated THBMEC with the inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma), which up-regulated chemokine and adhesion molecule expression in THBMEC without affecting the distribution of immunoreactivity for tight junction-associated proteins. PBMC adhesion was enhanced by cytokine-mediated activation of THBMEC. G protein-coupled receptor (GPCR) activation was essential for leukocyte-THBMEC interaction, as pertussis toxin (PTX) treatment of PBMC abrogated PBMC adhesion to activated THBMEC. The anti-alpha4 integrin antibody, natalizumab, infused into MS patients, significantly reduced the adhesion of their ex vivo PBMC to activated THBMEC under flow conditions. Further study showed that alternatively spliced fibronectin containing the CS1 region (FN-CS1), but not Vascular Cell Adhesion Molecule type 1 (VCAM-1), was the ligand of alpha4 integrin on activated THBMEC. Blocking FN-CS1 abrogated PBMC adhesion on activated THBMEC, while anti-VCAM-1 antibodies had no effect. These results established a novel in vitro dynamic BBB model. We also demonstrated the dependence of leukocyte-endothelial interactions in this model on alpha4 integrins and FN-CS1.
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PMID:alpha4 Integrin/FN-CS1 mediated leukocyte adhesion to brain microvascular endothelial cells under flow conditions. 1934 24

Mesenchymal stem cells (MSCs) have both multi-lineage differentiation potential and immunosuppressive properties, making them ideal candidates for regenerative medicine. However, their immunosuppressive properties potentially increase the risk of cancer progression and opportunistic infections. In this study, MSCs isolated from human umbilical cord blood (UCMSCs) and adult bone marrow (BMMSCs) were infected with human cytomegalovirus (HCMV). Cytopathic changes were observed 10 days post infection. PCR products amplified from genomic DNA and cDNA were used to confirm the HCMV infection of the UCMSCs and BMMSCs. Real-time PCR was conducted to quantify the expression of immunomodulatory molecules, including cytokines, chemokines, growth factors, adhesion molecules and cancer-related genes. Our results indicate high upregulation of the majority of these molecules, including many growth factors, tumor necrosis factor alpha, interleukin-8, interleukin-6 and interferon gamma. Adhesion molecules (VCAM-1, TCAM-1 and selectin-E) were downregulated in the infected UCMSCs and BMMSCs. Antibody chip array evaluation of cell culture media indicated that the growth factor secretion by UCMSCs and BMMSCs was greatly influenced (p < 0.001) by HCMV. The stimulation of MSCs with HCMV led to the activation of downstream signaling pathways, including pSTAT3 and Wnt2. Our results show that HCMV can significantly alter the functions of both UCMSCs and BMMSCs, although not in the same way or to the same extent. In both cases, there was an increase in the expression of proangiogenic factors in the microenvironment following HMCV infection. The discrepancy between the two cell types may be explained by their different developmental origin, although further analysis is necessary. Future studies should decipher the underlying mechanism by which HCMV controls MSCs, which may lead to the development of new therapeutic treatments.
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PMID:Gene expression profiles of various cytokines in mesenchymal stem cells derived from umbilical cord tissue and bone marrow following infection with human cytomegalovirus. 2456 81