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

Adhesion molecules are involved in the recruitment of leucocytes to sites of inflammation. In this study, we determined the expression of several adhesion molecules on isolated human alveolar type II pneumonocytes. Type II pneumocytes were isolated from 10 normal lung specimens, by enzymatic digestion with dispase, followed by metrizamide gradient centrifugation and panning on immunoglobulin G (IgG)-coated plastic dishes. With the freshly isolated type II cells, immunostaining was performed using a sensitive immunoperoxidase slide technique. In all cases, 60-90% of type II cells were positive for intercellular adhesion molecule-1 (ICAM-1) (CD54). A minor portion of type II cells expressed the alpha 4 (CD49d) subunit of the beta 1-integrins, and the alpha-v (CD51) subunit of the vitronectin receptor. CD11a, CD11b, CD11c, CD18, CD49b, and CD49f failed to demonstrate any immunostaining with type II cells. In conclusion, the observation of the expression of ICAM-1 and, to a lesser degree, of some integrin subunits, may indicate that alveolar type II cells participate in local immune and inflammatory responses.
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PMID:ICAM-1 and integrin expression on isolated human alveolar type II pneumocytes. 791 65

Adhesion molecules on the endothelium and leukocytes are involved in mediating cell-cell adhesion, which is an initial step in the leukocyte migration response. These adhesion molecules, some of which are present constitutively and others that can be up-regulated in response to chemotactic and proinflammatory stimuli, regulate the trafficking of leukocytes across the vascular endothelial barrier. A basic mechanism of interaction between the endothelium and leukocytes involves CD11/CD18 integrins, which bind to members of the immunoglobulin super gene family-intercellular adhesion molecule (ICAM)-1 and ICAM-2. The interaction between CD11/CD18 integrins and ICAM-1 is required for leukocyte migration. The other important adhesive interaction between leukocytes and the endothelium involves binding of selectins to their endothelium carbohydrate counterreceptors on leukocytes. The selectin-mediated binding is involved in leukocyte "rolling," whereas CD11/CD18 integrins are responsible for strengthening and stabilizing the leukocyte adhesion. This review summarizes the current literature on leukocyte adhesion molecules, in particular, the endothelial cell interactions mediated by the CD11/CD18 integrins.
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PMID:Endothelial cell interactions and integrins. 792 92

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

Ten small cell lung carcinoma and 12 non-small cell lung carcinoma cell lines of various histological types were studied for constitutive expression of the intercellular adhesion molecule-1 (ICAM-1). ICAM-1 was present in all squamous and large cell carcinoma cell lines whereas two out of five adenocarcinoma and all small cell lung cancer (SCLC) cell lines showed no basal ICAM-1 expression. ICAM-1 expression was upregulated by tumour necrosis factor-alpha (TNF-alpha) in a time- and dose-dependent manner in cell lines with basal ICAM-1 expression. Western blot analysis revealed a molecular size of 85 kDa for ICAM-1 in all but one cell line. The TNF-alpha-induced upregulation of ICAM-1 occurs on the transcriptional level. Adhesion of peripheral blood mononuclear cells to lung tumour cell lines could be inhibited by monoclonal antibodies (MAb) (CD11a;CD18) against the receptor of ICAM-1, the leukocyte function-associated antigen-1 (LFA-1), but not by a MAb (CD54) against ICAM-1 itself.
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PMID:Differential expression of the intercellular adhesion molecule-1 (ICAM-1) in lung cancer cell lines of various histological types. 811 Apr 95

We investigated 49 acquired immunodeficiency syndrome-related lymphomas (ARLs) for Epstein-Barr virus (EBV) by Southern blotting and in situ hybridization and, in positive cases, used cryostat immunohistology to compare EBV-latent gene expression (EBV encoded small RNA-1 [EBER-1], EBV nuclear antigen-2 [EBNA-2], latent membrane protein-1 [LMP-1] and host cell immunophenotype (CD11a, CD18, CD54, CD58, CD21, CD23, CD30, CD39, CDw70, immunoglobulin) patterns with those reported in other EBV infections. EBV+ immunoblast-rich/large cell ARLs (n = 22) showed three patterns of latency: broad (EBER+EBNA-2+/LMP-1+; n = 9), reminiscent of a lymphoblastoid cell line phenotype; restricted (EBER+/EBNA-2-/LMP-1-; n = 6), similar to endemic Burkitt's lymphoma; and intermediate (EBER+/EBNA-2-/LMP-1+; n = 7), a pattern rarely described in vitro but seen in certain EBV-related malignancies. EBNA-2 expression was associated with extranodal lymphomas. EBV+ Burkitt-type ARLs (n = 11) usually showed the restricted latency pattern (n = 8), but some expressed the intermediate form (n = 3). Adhesion (CD54, CD58) and activation (CD30, CD39, CDw70) molecule expression varied with morphology (immunoblast-rich/large cell versus Burkitt-type), but was not independently correlated with EBV-positivity. CD30 and LMP-1 expression were associated. ARLs show heterogeneity regarding both the presence of EBV and latency pattern. Comparison of these phenotypically distinct lymphoma groups with known forms of EBV infection provides clues to their possible pathogenesis.
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PMID:Epstein-Barr virus-latent gene expression and tumor cell phenotype in acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma. Correlation of lymphoma phenotype with three distinct patterns of viral latency. 821 3

Surface phenotypes and adhesion activity to human umbilical vein endothelial cells (HUVECs) were studied using leukemic cells from 12 Japanese patients with B-cell chronic lymphoid leukemias including 7 with chronic lymphocytic leukemia (CLL), 1 with prolymphocytic leukemia (PLL), 2 with hairy cell leukemia (HCL) and 2 with HCL variant (HCL-V). CD13 and CD23 were found to be characteristically positive in CLL, whereas they were not expressed in non-CLL cases except for positivity of CD23 in two such cases. Except for CD11b, all other leukocyte integrins examined (CD11a, CD11c and CD18) and their ligand (CD54) were highly expressed in non-CLL cases. Adhesion activity of leukemic cells to HUVECs after co-culture with HUVECs was well correlated with the expression of CD11b, CD18 and CD54, but showed no predilection for any leukemia subtype. Positivity for CD5, CD21, CD23 and CD13 changed after the co-culture with HUVEC. These results suggest that adhesion activity after co-culture. does not correlate with the leukemia subtype and that endothelial cells activate or differentiate leukemic cells.
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PMID:Surface phenotype and adhesion activity of B-cell chronic lymphoid leukemias. 822 Jan 19

Extravasation of leukocytes at the sites of ischemia-reperfusion is thought to exacerbate the tissue injury. It has been proposed that leukocyte accumulation is a secondary effect of the ischemic damage, mediated by inflammatory cytokines. We have recently demonstrated that physiologically low levels of oxygen tension alone can have a direct effect on the adhesive characteristics of mesenchymal cells for lymphocytes. We now report that decrease of oxygen tension in the environment induces the adhesion of neutrophils to human endothelial cells in culture. Adhesion of human neutrophils to human umbilical vein, bovine aortic, and mouse microvascular endothelial cell monolayers, which had been incubated at pO2 of 50 torr for 3 hours, increased 2.5-fold, 2-, and 1.5-fold, respectively. The effects of decreased oxygen concentration on adhesion were not mediated by a soluble factor elaborated by the hypoxic cells. Low oxygen tension upregulates a saturable, endothelial cell-associated adhesion mechanism, capable of withstanding centrifugation forces greater than 160g. Hypoxia-induced adhesion was inhibited by LFA-1-specific (CD11a/CD18 integrin) antibodies, but not by antibodies directed against the ICAM-1 ligand for the LFA-1 receptor. These studies demonstrate that decreases in oxygen tension alone increase the adhesive properties of endothelial cells for leukocytes. In addition, they provide evidence for the existence of a new ligand for the LFA-1 molecule on endothelial cells which can be affected by hypoxic environments.
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PMID:Oxygen tension regulates neutrophil adhesion to human endothelial cells via an LFA-1-dependent mechanism. 825 69

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

Adhesion of parasitized red blood cells to vascular endothelium is thought to play an important role in the development of the ischaemic complications associated with severe falciparum malaria. Using a novel, flow-based assay, we have investigated the adhesion of parasitized red blood cells to formalin-fixed human umbilical vein endothelial cells (HUVEC), for isolates obtained from 32 Gambian subjects with mild or severe falciparum malaria. Red cells infected with wild strains of Plasmodium falciparum were able to adhere to HUVEC under physiologically relevant flow conditions, but the level of adhesion was highly variable, ranging from 1 to 688 adherent cells per mm2 of HUVEC. Within isolates, some adherent parasitized cells remained stationary, whilst other formed less stable interactions and rolled slowly over the cell surface. There was no significant difference in adhesion of parasitized cells between isolates obtained from mild or severe cases of malaria, although a subset of isolates did show very high levels of adhesion. The results suggest that there is not a simple relationship between the adhesion of parasitized cells to cultured endothelial cells (presumably via the receptor ICAM-1) and the clinical severity of the disease, although variation in microvascular adhesion in vivo may still be a determinant of ischaemic complications.
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PMID:Adhesion of parasitized red blood cells to cultured endothelial cells: a flow-based study of isolates from Gambian children with falciparum malaria. 827 17


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