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

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

Eosinophils are recruited to the site of IgE-mediated allergic reaction in the airway in asthma. Major eosinophil-chemotactic factors released from mast cells are platelet activating factor and Leukotriene B4. In addition, T cells and bronchial epithelial cells produce eosinophil chemotactic cytokines. Cytokines including IL-5, IL-3, and GM-CSF, which are released mainly from CD4+ T cells and possibly Th2, activates eosinophils for migration, tissue damage, and survival. Adhesion molecules on eosinophils and constituent structures of the airway participate in the process of eosinophil migration. Among a variety of adhesion molecules, VLA-4 and VCAM-1 are unique to the interaction between eosinophils and endothelial cells. A major role of recruited eosinophils in the airway in asthma is considered to be damage to the bronchial epithelium caused by eosinophil specific granules proteins, in addition to production of lipid mediators, production of cytokines, antigen-presenting cell function, and possible induction of basement membrane thickening in the airway.
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PMID:Eosinophils and allergy in asthma. 776 55

We have previously shown that lymphocytic cells bind to cultured syncytiotrophoblast and that this may be important in the lymphocyte-mediated infection of trophoblast with the human immunodeficiency virus (HIV). Leukocyte-trophoblast adhesion may also have implications for normal trophoblast function. The following experiments were designed to characterize the adhesion systems that mediate the attachment of lymphocytic cells to trophoblast. Adhesion was assayed by labelling lymphocytic MOLT-4, clone 8 cells with the fluorescent marker, calcein-AM, and then incubating them with primary cultures of human syncytiotrophoblast. Adhesion was stimulated by pretreatment of the trophoblast cultures with several cytokines either alone or together. These included tumor necrosis factor-alpha (TNF-alpha), granulocyte/macrophage-colony stimulating factor (GM-CSF), interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma). Stimulation was time- and dose-dependent. In contrast, preincubation of trophoblast cultures with anti-TNF-alpha antibodies for 2 days reduced MOLT adhesion by almost 50%. Preincubation with other anti-cytokine antibodies had no significant effect on adhesion. In other experiments, adhesion was measured in the presence of antibodies to known adhesion molecules. Adhesion was reduced by 50% in the presence of antibodies to alpha 4 integrin or beta 1 integrin. When present together, these antibodies reduced adhesion by almost 85%. Incubation in the presence of antibodies to the very late activation antigen-4 (VLA-4; alpha 4 beta 1 integrin) counter-receptors, VCAM-1 and CS-1, was without effect. Adhesion was also unaffected by antibodies to LFA-1, ICAM-1, ICAM-2, LFA-2, or LFA-3. These results suggest that adhesion is mediated by an adhesion system consisting of lymphocyte VLA-4 (alpha 4 beta 1) and an as yet unidentified counter receptor on trophoblast.
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PMID:Effect of cytokines and anti-adhesion molecule antibodies on the adhesion of lymphocytic cells to human syncytiotrophoblast. 780 71

The mechanisms responsible for the accumulation of eosinophils at sites of allergic and other inflammatory reactions are unknown, but recent studies have implicated both eosinophil and endothelial adhesion molecules in this process. However, less well studied have been the adhesive interactions between eosinophils and the subendothelial basement membrane and interstitial connective tissues. To test the hypothesis that eosinophils might interact with extracellular matrix proteins, we analyzed purified human eosinophils for the expression and function of various beta 1 integrins. Using indirect immunofluorescence and flow cytometry, purified eosinophils from mildly allergic donors were found to consistently express the integrin subunits beta 1 (CD29), alpha 4 (CD49d, very late activation antigen [VLA]-4 alpha), and alpha 6 (CD49f, VLA-6 alpha). No significant expression of the alpha 1, alpha 2, alpha 3, alpha 5, or beta 4 subunits was detected. Platelet contamination of the eosinophil preparations was excluded by light microscopy and by the inability to detect expression of platelet glycoproteins alpha v, CD41b, and CD42b. Immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of eosinophils confirmed the expression of cell-surface beta 1, alpha 4, and alpha 6. Furthermore, eosinophils purified from allergic donors were shown to adhere to plate-bound laminin, but not to type 1 or type 4 collagen. Adhesion to laminin was concentration-dependent, required divalent cations, and was completely and specifically inhibited by the anti-alpha 6 monoclonal antibody (MoAb) GoH3 and by the anti-beta 1 MoAb 33B6. Interestingly, the anti-beta 1 MoAb 18D3 (which like 33B6 blocks eosinophil binding to VCAM-1) did not inhibit eosinophil adhesion to laminin, suggesting that there are functionally distinct epitopes on the beta 1 subunit. Eosinophils purified from 4 healthy, nonallergic donors also showed alpha 6-dependent adhesion to laminin, although these cells adhered less well. These studies establish the expression of alpha 6 beta 1 on human eosinophils and document its function as a laminin receptor. Interaction of eosinophil alpha 6 beta 1 with laminin, eg, in basement membranes, may contribute to the localization of these cells at inflammatory sites in vivo.
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PMID:Expression of a functional laminin receptor (alpha 6 beta 1, very late activation antigen-6) on human eosinophils. 821 35

Adhesion between leukemic cells and the vascular endothelium has been suggested to play a role in the development of leukostasis in myelocytic leukemia. To define the role of adhesion molecules on the surface of endothelial cells in leukostasis, we used immunohistochemistry to study the expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in lung tissue of 4 patients with pulmonary leukostasis. Lung tissue of 2 patients with myelocytic leukemia without leukostasis and 4 patients with irrelevant nonpulmonary disease was used as a negative control. Positive control tissues included a lymph node with angioimmunoblastic lymphadenopathy and a hyperplastic tonsil. Weak positive staining for ELAM-1 was found in 1 patient in vessels, both with and without leukostasis. Expression of VCAM-1 and ICAM-1 in all patients tested was similar to that in the negative controls. The results of this study suggest that activation of endothelium, with increased expression of the endothelial adhesion molecules under study, is not a prerequisite for the development of pulmonary leukostasis in leukemia.
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PMID:Endothelial activation antigens in pulmonary leukostasis in leukemia. 823 71

It has been demonstrated that: a) part of the inhalant allergenic particles we normally breath, adhere to the oropharyngeal mucosa, and eventually progress to the gastrointestinal tract; b) digestive tract mucosa is able to produce specific IgE against aeroallergens even before than respiratory tract mucosa. The case is described of a 5-year-old girl who presented a daily vomiting since she was 6 months. All clinical instrumental and laboratory findings had been unable to reach a definite diagnosis. SPT (inhalants and foods): Dermatoph. pteronyssinus: + (confirmed by RAST). The patient had an immediate, complete recover just following the clinician's instruction for HDM domestic prevention. Symptoms appeared again in response to a NPT performed with Dermatophagoides extract. The positivity of the exclusion-re-exposure test confirmed the diagnosis of HDM-induced gastrointestinal allergic syndrome, so far not described in literature (to my knowledge). Immunological considerations: since it is known that patients allergic to HDM do not usually present a specific IgE-mediated gastrointestinal allergic syndrome, it is suspectable that an immunological tolerance can be instaured toward inhalant allergens as it normally happens toward food allergens. In atopic individuals there is a high expression of ICAM-1, VCAM-1 and other adhesion molecules on the surface of HEV at BALT level. Adhesion molecules expression and immunocompetent cells activation are modulated by several mechanisms among which the cytokine network plays a major role. The author speculates that sensitized lymphocytes may migrate from intestinal to bronchial mucosa, via lymphocytic immunoallergic competence. In the described clinical case this mechanism did not work.
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PMID:[Habitual vomiting due to dust mite allergy. A case report]. 826 65

It is now clear that adhesive interactions play a critical role in the process of metastatic tumor dissemination. Adhesion molecules act as both positive and negative modulators of the metastatic process. Molecules such as E-cadherin that promote homotypic tumor cell adhesion function to maintain intercellular contacts that confine cells to the primary tumor site and are negatively correlated with metastatic potential. Because tumor cells are rapidly eliminated from the circulation, those cells that can quickly arrest in the vasculature at a secondary site and pass through the vessel wall into the surrounding tissue will have a selective advantage toward establishing new metastatic colonies. The first step in this process is specific adhesion to venular endothelial cells in selected organs, a process mediated by tumor cell surface molecules such as Sialyl LewisX or the VLA-4 (alpha 4 beta 1) integrin that mediate binding to endothelial adhesion molecules such as the E-selectin or the vascular cell adhesion molecule, VCAM-1. Site-specific endothelial determinants such as the lung endothelial cell adhesion molecule, LuECAM, may additionally specify particular sites for preferential adhesion and subsequent site-specific metastasis of particular tumor types. After adherence to endothelial cells and subsequent endothelial retraction, metastatic tumor cells must adhere to elements of the subendothelial basement membrane such as laminin and types IV and V collagen, interactions frequently mediated by members of the beta 1 and beta 4 integrin families. Finally, metastatic tumor cell adhesion to connective tissue elements such as fibronectin, type I collagen and hyaluronan, mediated by molecules such as the beta 1 integrins and by the CD44 cell surface adhesion molecule, are required for movement of tumor cells into the subendothelial stroma and subsequent growth at these new sites. Thus, metastatic potential can be influenced both positively and negatively by a variety of cell surface adhesive molecules that act both independently and in concert to direct tumor cells to particular tissues, allowing them to arrest in those tissues, migrate across the vessel wall and grow at the secondary site. In the current review, I discuss the nature of the adhesion molecules that have been implicated in the metastatic process, emphasizing those molecules that have been shown to correlate with metastasis in clinical human tumors or that have been shown to influence metastatic potential in in vivo experimental assays.
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PMID:Adhesion molecules in tumor metastasis. 840 Jan 43

Cell-cell adhesion is essential for many immunological functions and is believed to be important in the regulation of hematopoiesis. Adhesive interactions between human endothelial cells and megakaryocytes were characterized in vitro using the CMK megakaryocytic cell line as well as marrow megakaryocytes. Although there was no adhesion between unactivated human umbilical vein endothelial cells (HUVEC) and megakaryocytes, treatment of HUVEC with inflammatory cytokines such as IL-1 beta, tumor necrosis factor alpha, INF-gamma, or the phorbol ester phorbol myristate acetate (PMA) resulted in a time- and dose-dependent increase in adhesion. Stimulation of marrow megakaryocytes or CMK cells with the cytokines IL-1 beta, GM-CSF, IL-6, IL-3, or PMA augmented their adhesion to endothelium. Monoclonal antibodies against the LFA-1 subunit of the leukocyte adherence complex CD18 inhibited the binding of marrow megakaryocytes or CMK cells to HUVEC. Adhesion blocking experiments also demonstrated that the VLA-4/VCAM-1 pathway was important for megakaryocyte attachment to HUVEC. Adhesion promoted maturation of megakaryocytic cells as measured by increased expression of glycoproteins GpIb and GpIIb/IIIa and by increased DNA content. These observations suggest that alterations in megakaryocyte adhesion may occur during inflammatory conditions, mediated by certain cytokines, resulting in augmented megakaryocyte maturation.
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PMID:Characterization of adhesive interactions between human endothelial cells and megakaryocytes. 851 51

Adhesion of peripheral blood eosinophil and neutrophil granulocytes to the endothelial cell adherence receptors E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 has been measured. The study included patients with allergic rhinitis, patients with mild allergic and nonallergic asthma, and healthy individuals; 10 persons were in each group. In addition, assay of eosinophil and neutrophil cell surface expression of the receptor complex CD11b/CD18 was performed. Increased eosinophil adhesion to vascular cell adhesion molecule-1 (p < 0.05) and intercellular adhesion molecule-1 (p < 0.05) was demonstrated in the patients with a more labile asthma, that is, a peak expiratory flow rate variability of more than 10%, suggesting a relationship to the degree of ongoing inflammation in the airways of the patients. The increased eosinophil adhesion was most probably due to a functional upregulation of the CD11b/CD18 and very late activation antigen-4 receptors, because the number of receptors measured as cell surface expression was unaltered. The increased eosinophil adhesion in the patients with high peak expiratory flow rate variability appeared independent of atopy. The increased adhesion was not entirely specific to the eosinophils, because neutrophils from patients with a peak expiratory flow rate variability of more than 10% also demonstrated increased adhesion to intercellular adhesion molecule-1 (p < 0.05) when compared with neutrophils from the patients with low peak expiratory flow rate variability. In conclusion, the demonstrated priming of eosinophil adhesion to vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 might be one contributing mechanism behind the selective accumulation of eosinophils in the lung tissue of patients with asthma.
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PMID:Increased adhesion to vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 of eosinophils from patients with asthma. 854 53

In renal biopsy specimens from 15 patients with antineutrophil cytoplasmic autoantibody (ANCA)-associated renal vasculitis, the infiltrating intraglomerular and interstitial leukocytes were localized and the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and the cytokine interleukin-1 alpha (IL-1 alpha) were studied by an immunohistochemical method. Intraglomerular leukocytes were mainly macrophages (13.46 +/- 9.29 cells/glomerular cross-section) and, to a lesser extent, T lymphocytes (4.61 +/- 2.81 cells/glomerular cross-section). Staining with VCAM-1, which was negative in the undamaged tufts, was strongly positive in necrotizing-extracapillary lesions. Staining with ICAM-1 was also present in the damaged tufts, but its pattern was more diffuse. Intraglomerular IL-1 alpha was found in all biopsy specimens. Where the Bowman's capsule was not damaged, the periglomerular infiltrating cells were macrophages (42.6 +/- 25.2 cells/glomerular cross-section) and T lymphocytes (51.06 +/- 33.0 cells/glomerular cross-section). When there was a granulomatous lesion involving the glomerulus, the number of cells per granulomatous area revealed a massive number of CD45-positive leukocytes (345.83 +/- 237.47 cells/granulomatous lesion), many of them positive for activity markers (HLA-DR, IL-2R), adhesion molecules, and IL-1 alpha. Many activated cells were also present in interstitial areas of perivascular clusters of leukocytes, in which T lymphocytes (prevalently CD4+ cells) outnumbered the macrophages (331.55 +/- 207.85 cells/0.05 mm2 area v 125.68 +/- 60.57 cells/0.05 mm2 area). Adhesion molecules and IL-1 alpha were found in both tubular and vascular areas in all biopsy specimens. Our data strongly support the involvement of both the adhesion molecules ICAM-1 and VCAM-1 in the recruitment of intraglomerular leukocytes in renal vasculitis, indicate that VCAM-1 is a very good marker of necrotizing-extracapillary damage, and suggest its crucial connection with the macrophage recruitment in these vasculitic lesions. The presence of histochemically detectable levels of IL-1 alpha in glomeruli, tubules, and vessels and on some inflammatory cells supports its involvement in the vasculitic lesions, probably by triggering a positive feedback that increases the damage.
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PMID:Intraglomerular and interstitial leukocyte infiltration, adhesion molecules, and interleukin-1 alpha expression in 15 cases of antineutrophil cytoplasmic autoantibody-associated renal vasculitis. 854 38


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