UMLS:C0001511 - FACTA Search

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

The adhesion of circulating leukocytes to the vascular endothelium is essential for effective host inflammatory and immune responses. Adhesion proteins expressed by both the leukocyte and endothelial cell have been well characterized, and studies of these molecules have shown that both cell types are actively involved in regulating these binding events. Most leukocyte (leukocyte integrins) and endothelial cell (vascular selectins, ICAM-1, and VCAM) adhesion proteins increase in expression and function in response to mediators released by inflamed tissues. In contrast, the expression and function of one type of leukocyte molecule, L-selectin (previously called LECAM-1, LAM-1, gp90MEL-14), is "down-regulated" by inflammatory signals. The purpose of this review is to summarize in vitro and in vivo regulatory and functional studies of some of the molecular mechanisms which regulate leukocyte-endothelial cell adhesion, with particular emphasis on L-selectin, and to present a hypothetical model of how these molecules may be orchestrated in vivo resulting in the control of host inflammatory responses.
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PMID:Leukocyte traffic to sites of inflammation. 137 85

Adhesion of isolated human polymorphonuclear granulocytes (PMNs) to five different phenotypes of cultured microvascular endothelial cells derived from bovine corpora lutea was investigated by measuring the myeloperoxidase content of cell lysates. Untreated and interleukin 1 (IL-1) -pretreated confluent monolayers were overlaid with unstimulated and phorbol ester (PMA)-stimulated PMNs in the absence and presence of the monoclonal antibody IB4 recognizing and functionally blocking beta 2 (CD18) of the leukocyte integrins. Unstimulated PMN adhesion was highest on type 4, followed by type 3 and 5 endothelial cells. This adhesion was not inhibited by treatment with IB4. IL-1 pretreatment of endothelial cells resulted in a significant increase of PMN adhesion on types 1, 2, and 4, most of which was also beta 2 integrin-independent. PMA-stimulation of PMNs increased adhesion to maximal values on cell types 1 and 5, which was largely blocked by IB4. Type 2 endothelial cells supported significantly less PMA-stimulated PMN adhesion than all other types. In the presence of IB4, adhesion of PMNs to untreated and IL-1-pretreated type 3 and 4 endothelial cells was significantly reduced by PMA. This reduction of beta 2 integrin-independent adhesion by PMA stimulation is compatible with possible shedding of the lectin-like leukocyte adhesion molecule, L-selectin, from PMNs. Differential PMN adhesion may reflect distinctive expression of endothelial adhesion molecules in different phenotypes of microvascular endothelial cells. Endothelial specialization within the microcirculation may have important functional consequences for the inflammatory response in vivo.
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PMID:Differential adhesion of granulocytes to five distinct phenotypes of cultured microvascular endothelial cells. 137 29

Neutrophil infiltration in synovial fluid is an important step in inflammation characterizing rheumatoid arthritis (RA). In this study, the activation and functional state of neutrophils in the blood and synovial fluid of patients with rheumatoid arthritis were compared: mean density of neutrophil activation markers CD11b, CD18 and L-selectin was measured with a flow cytometer, and adhesion to chondrocytes using a fluorimetric assay. No significant differences between control and patient peripheral blood neutrophils were observed. When comparing neutrophils of patient peripheral blood with paired synovial fluid, an increase in CD11b (p = 0.008) and a decrease in L-selectin (p = 0.008) were measured. For neutrophils of control and patient peripheral blood, fMet-Leu-Phe stimulation induced upregulation of CD11b (resp p = 0.007 and p = 0.008) and CD18 (resp p = 0.005 and p = 0.01). In the synovial fluid, no significant increase in CD11b and CD18 could be induced with fMet-Leu-Phe. Percentages of adherent neutrophils were comparable between controls and patients, both in peripheral blood and synovial fluid. Adhesion to chondrocytes of peripheral blood neutrophils of patients was correlated with clinical (Ritchie) and biological (erythrocyte sedimentation rate) parameters (resp r = 0.67, r = 0.73). In conclusion, these results demonstrate that peripheral blood neutrophil adhesion to chondrocytes was correlated with active disease, and that synovial fluid neutrophils were activated in vivo. These findings provide further evidence for the contributing role of neutrophils in articular destruction in RA.
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PMID:Expression of neutrophil activation markers and neutrophil adhesion to chondrocytes in rheumatoid arthritis patients: relationship with disease activity. 748 Oct 76

In this study direct immunofluorescence and flow cytometry with calibration using quantitative bead standards were used to enumerate the cell surface receptors CD11a/CD18, CD11b/CD18 and L-selectin. Holding blood at room temperature and fixation of samples prior to staining induced changes in expression, while immediate staining of polymorphonuclear granulocytes (PMN) in whole blood followed by fixation produced accurate values. The ranges of PMN adhesion molecule expression in 10 normal individuals were CD11a/CD18: 14794-28725, CD11b/CD18: 5300-11939 and L-selectin: 35662-61654 receptors per cell. Differences within individuals over 4 h were also observed. Adhesion molecule expression is used as an index of the adhesive function and state of activation of the cell. The data presented here shows that there is inherent variability in the expression of the PMN adhesion molecules between and within individuals, thus direct comparisons of PMN adhesion molecule expression between patients and "normals" must be interpreted with caution.
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PMID:Polymorphonuclear granulocyte expression of CD11a/CD18, CD11b/CD18 and L-selectin in normal individuals. 751 31

Adhesion molecules facilitate infiltration of leukocytes into the central nervous system (CNS) of mice with experimental allergic encephalomyelitis (EAE). Expression of the adhesion molecules ICAM-1 (CD54), VCAM-1 (CD106), L-selectin (CD62L), and leukosialin (CD43) was analyzed via immunocytochemistry 4-28 days after the injection of encephalitogen into EAE-susceptible SWXJ mice. Constitutive ICAM-1 expression on large-diameter CNS vessels was upregulated on post-injection days 8, 11, 14 and 18 (concurrent with de novo expression on smaller capillaries and glial cells), partially downregulated by day 23, and back to control levels by day 28. Constitutive VCAM-1 expression was upregulated by day 14 and back to control levels by day 28. Upregulation of ICAM-1 temporally coincided with the immigration of CD4+ lymphocytes and L-selectin+ leukocytes into the CNS, while downregulation coincided with their emigration. The infiltration of CD43+ leukocytes also coincided with the upregulation of vascular adhesion molecules, but CD43+ cells remained in the CNS after ICAM-1 and VCAM-1 had returned to control levels. Cellular infiltration and adhesion-molecule expression preceded EAE clinical symptoms by a minimum of 3 days, suggesting a causal role of adhesion molecules in the initiation of CNS inflammation. However, prophylactic injections of monoclonal antibodies against either ICAM-1, L-selectin, or CD43, did not ameliorate the clinical severity of EAE in this model.
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PMID:Expression of ICAM-1, VCAM-1, L-selectin, and leukosialin in the mouse central nervous system during the induction and remission stages of experimental allergic encephalomyelitis. 752 43

Understanding the molecular mechanisms of pulmonary lymphocyte recruitment is a crucial step toward selective control of immune lung diseases and infections in immunocompromised hosts. To dissect these mechanisms, we are studying the response induced in primed C57BL/6 mice by intratracheal challenge with the T cell-dependent antigen, sheep red blood cells (SRBC). This study used four-parameter flow cytometry to examine expression by CD4+ murine T cells in peripheral blood and lungs of receptors known to be differentially expressed on primed human lymphocytes (CD2, CD11a, CD44, CD45RB, CD49d, and L-selectin). Compared with peripheral blood, more lung CD4+ T cells recovered by bronchoalveolar lavage (BAL) showed a primed phenotype. Judged by low expression of CD45RB or L-selectin, 76 to 90% of BAL CD4+ T cells were primed at all times. Adhesion receptor phenotype of CD4+ T cells in BAL and lung interstitium agreed closely, although BAL contained a greater percentage of primed cells. The percentage of CD4+ T cells with high expression of CD44+ and CD49d increased late in the response. However, when considering only upregulated adhesion receptors which might mediate recruitment, 22 to 52% of CD4+ T cells in BAL did not have increased adhesion receptor expression. Longer duration between priming and challenge did not increase adhesion receptor upregulation. High adhesion receptor expression was least evident during the periods of maximal lymphocyte influx, suggesting that factors other than increased surface density of organ-nonspecific adhesion receptors contribute to lymphocyte recruitment during pulmonary immune responses.
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PMID:Adhesion receptor phenotypes of murine lung CD4+ T cells during the pulmonary immune response to sheep erythrocytes. 753 69

Adhesion molecules play a role in the migration of hematopoietic progenitor cells and regulation of hematopoiesis. To study whether the mobilization process is associated with changes in expression of adhesion molecules, the expression of CD31, CD44, L-selectin, sialyl Lewisx, beta 1 integrins very late antigen 4 (VLA-4) and VLA-5, and beta 2 integrins lymphocyte function-associated 1 and Mac-1 was measured on either bone marrow (BM) CD34+ cells or on peripheral blood CD34+ cells mobilized with a combination of granulocyte colony-stimulating factor (G-CSF) and chemotherapy. beta 1 integrin VLA-4 was expressed at a significantly lower concentration on peripheral blood progenitor cells than on BM CD34+ cells, procured either during steady-state hematopoiesis or at the time of leukocytapheresis. No differences in the level of expression were found for the other adhesion molecules. To obtain insight in which adhesion molecules may participate in the homing of peripheral blood stem cells (PBSCs), the number of CD34+ cells expressing these adhesion molecules present in leukocytapheresis material was quantified and correlated with hematopoietic recovery after intensive chemotherapy in 27 patients. The number of CD34+ cells in the subset defined by L-selectin expression correlated significantly better with time to platelet recovery after PBSC transplantation (r = -.86) than did the total number of CD34+ cells (r = -.55). Statistical analysis of the relationship between the number of CD34+L-selectin+ cells and platelet recovery resulted in a threshold value for rapid platelet recovery of 2.1 x 10(6) CD34+ L-selectin+ cells/kg. A rapid platelet recovery (< or = 14 days) was observed in 13 of 15 patients who received > or = 2.1 x 10(6) CD34+ L-selectin+ cells/kg (median, 11 days; range, 7 to 16 days), whereas 10 of 12 patients who received less double positive cells had a relative slow platelet recovery (median, 20 days; range, 13 to 37 days). The L-selectin+ subpopulation of CD34+ cells also correlated better with time to neutrophil recovery (r = -.70) than did the total number of reinfused CD34+ cells (r = -.51). However, this latter difference failed to reach statistical significance. This study suggests that L-selectin is involved in the homing of CD34+ cells after PBSC transplantation.
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PMID:Expression of adhesion molecules on CD34+ cells: CD34+ L-selectin+ cells predict a rapid platelet recovery after peripheral blood stem cell transplantation. 753 23

Adhesion of neutrophils, lymphocytes and promyelocytic HL60 cells was compared in a flow-based model in which a monolayer of activated platelets formed the adhesive substrate. Each type of leucocyte formed P-selectin-mediated rolling attachments on the platelet surface under physiologically relevant flow conditions. Lymphocytes adhered less, and HL60 in similar numbers, compared to neutrophils, whereas the lymphocytes and HL60 cells rolled much more rapidly. Sulphated, sialylated saccharide(s) were implicated as ligand(s) for P-selectin for all leucocytes, but L-selectin (borne by neutrophils and lymphocytes, but not HL60 cells) appears to be a major presenter of ligand for neutrophils alone. T cells enriched from peripheral blood lymphocytes adhered in greater numbers than B cells. Differentiation of HL60 cells to neutrophil-like cells (induced by DMSO) caused cell volume to decrease and surface expression of integrin adhesion molecules to increase, but only a small percentage of cells were converted to an L-selectin-bearing phenotype. Differentiated cells showed evidence of stabilization of adhesion with increasing stress and a marked reduction in rolling velocity. These studies indicate that cell differentiation may be accompanied by alteration of adhesive behaviour, resulting from changes in physical characteristics as well as surface properties. Moreover, results suggest that P-selectin could promote lymphocyte attachment to endothelium in acute inflammatory conditions and possibly mediate lymphocyte-platelet interaction during thrombosis.
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PMID:Adhesion of flowing leucocytes to immobilized platelets. 753 23

Adhesion molecules are important in T-cell trafficking to sites of inflammation. We determined levels of circulating vascular cell adhesion molecule-1 (VCAM-1), L-selectin, and E-selectin in the serum of 147 patients with definite multiple sclerosis of the remitting-relapsing or secondary progressive type. Soluble VCAM-1 and L-selectin concentrations were increased compared to levels in a large group of control subjects. Levels were highest in patients with gadolinium-enhancing lesions on magnetic resonance imaging (VCAM-1: 1,011 +/- 276 vs 626 +/- 87 ng/ml; L-selectin: 1,130 +/- 272 vs 793 +/- 207 ng/ml [mean +/- standard deviation]; p < 0.0001 vs patients without enhancing lesions). Serum levels of soluble tumor necrosis factor receptor (60 kd) were also raised (2.64 +/- 1.23 vs 2.17 +/- 0.69 ng/ml in subjects with other neurological diseases and 2.1 +/- 0.77 ng/ml in healthy control subjects; p < 0.05). Soluble VCAM-1 and L-selectin levels were correlated to concentrations of soluble tumor necrosis factor receptor. In 13 patients with viral encephalitis, similar observations were made. Raised levels of soluble VCAM-1 and L-selectin probably reflect cytokine-induced endothelial cell and T-lymphocyte/monocyte activation occurring in the process of T-cell migration into the central nervous system. Tumor necrosis factor-alpha may be critically involved.
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PMID:Circulating adhesion molecules and tumor necrosis factor receptor in multiple sclerosis: correlation with magnetic resonance imaging. 754 73

Interaction between neutrophils and platelets at the site of vascular damage or in ischaemic tissue may promote thrombosis and/or vascular occlusion. To study this interaction, we have developed a novel technique that allows visualization of adhesion of flowing neutrophils to immobilized, activated platelets. The total number of adherent neutrophils decreased with increasing wall shear stress in the range 0.05 to 0.4 Pa. Although a proportion of the adherent neutrophils were stationary, most were rolling with a velocity greater than 0.4 micron/s. The percentage of rolling cells increased with increasing wall shear stress, but the mean rolling cell velocity was nearly independent of shear stress. Adhesion of neutrophils was nearly abolished by treatment of the platelets with antibody to P-selectin, or by treatment of neutrophils with either neuraminidase, dextran sulfate, or EDTA. Studies with a series of antibodies to L-selectin (TQ-1, Dreg-56, LAM1-3, and LAM1-10) suggested that this molecule was one neutrophil ligand for rolling adhesion. Thus, sialylated carbohydrate on neutrophils appears essential for P-selectin-mediated adhesion, and a proportion of this ligand may be presented by L-selectin. Treatment of the neutrophils with N-formyl-methionyl-leucyl-phenylalanine decreased the number of rolling cells, and increased the rolling velocity, possibly due to shedding of neutrophil ligand(s) and/or cell shape change. In vivo, immobilized platelets could play an important role in promoting attachment of neutrophils to vessel walls, eg, by slowing neutrophils so that integrin-mediated immobilization could occur.
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PMID:Selectin-mediated rolling of neutrophils on immobilized platelets. 768 89

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