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)

Adhesion of activated natural killer (A-NK) cells to activated and nonactivated endothelial cells in vitro was studied under dynamic flow conditions. Endothelial cells grown on glass slides were either treated with tumor necrosis factor-alpha (TNF alpha) or medium, then placed into a flow chamber over which suspensions of A-NK cells were passed using a range of defined shear stress levels. Significant numbers of binding cells could be consistently observed at shear stress levels less than 3 dyn/cm2 on TNF alpha-activated endothelium or at 0.59 dyn/cm2 on nonactivated endothelium. Stable adhesion occurred rapidly following the initial interaction of the following cells with the endothelium in the absence of detectable rolling. Pretreatment of the A-NK cells with monoclonal antibodies directed against CD18 (LFA-1) or CD49d (VLA-4) resulted in a significant reduction in the number of binding cells. Simultaneous treatment with both monoclonal antibodies eliminated all A-NK adhesion occurring over 0.5 dyn/cm2. Pretreatment of the endothelial cells with antibodies against E- or P-selectin resulted in a small but significant reduction in binding only at 0.5 dyn/cm2. The binding efficiency of the A-NK cells was similar to that previously observed for T lymphocytes under the same conditions. Once bound, approximately half of the adherent cells could resist detachment when exposed to wall shear stresses over 12 dyn/cm2. These findings indicate that A-NK cell adhesion to activated endothelium can occur under shear stress conditions which are representative of postcapillary venules and that this binding is mediated principally by both CD18 and CD49d. A-NK cell adhesion also occurs to nonactivated endothelium but only at wall shear stress levels less than 1 dyn/cm2.
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PMID:Adhesion of activated natural killer cells to tumor necrosis factor-alpha-treated endothelium under physiological flow conditions. 916 65

Adhesion of leukocytes to vascular endothelium is crucial for leukocyte migration into tissues. The contributions of L-selectin, P-selectin, and ICAM-1 to interactions between lymphocytes and endothelium was examined using allogeneic skin graft rejection as a model of cutaneous inflammation. L-selectin-deficient (L-selectin(-/-)) mice rejected both primary and secondary allogeneic (BALB/c) skin grafts significantly more slowly than L-selectin(+/+) littermates. Furthermore, skin graft rejection remained significantly delayed in L-selectin(-/-) mice, despite placement of grafts 7 days after i.p. immunization with allogeneic cells, when CTL responses in L-selectin(-/-) mice and L-selectin(+/+) littermates were confirmed to be equivalent. Indeed, specific CTL responses to BALB/c splenocytes were normal or elevated in L-selectin(-/-) mice following either skin grafts or immunization. However, the number of T lymphocytes within allogeneic grafts was lower in L-selectin(-/-) mice as compared with L-selectin(+/+) littermates. Therefore, delayed rejection of skin grafts by L-selectin(-/-) mice reflects impaired migration of effector cells into the graft rather than delayed or impaired generation of a CTL response. In contrast to L-selectin(-/-) mice, P-selectin-deficient and ICAM-1-deficient mice rejected allogeneic skin grafts normally. These findings delineate an important role for L-selectin in lymphocyte recruitment to cutaneous sites of inflammation.
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PMID:L-selectin is involved in lymphocyte migration to sites of inflammation in the skin: delayed rejection of allografts in L-selectin-deficient mice. 916 36

Oxidants generated by endothelial xanthine oxidase (XO) can help trigger free radical-mediated tissue injury. An important event in oxidant-mediated tissue injury is neutrophil-endothelial adhesion. Although activation of endothelial XO increases adhesion, little is known about xanthine in the adhesive effect of XO. This study examined administered xanthine on the adhesion of neutrophils. Endothelial [human umbilical vein endothelial cells (HUVEC)] monolayers were exposed to xanthine (15 min), and neutrophils were allowed to adhere to HUVEC in an adhesion assay. Adhesion was dose dependently increased by xanthine (3-100 microM). Either catalase (1,000 U/ml), oxypurinol (XO inhibitor; 100 microM), or platelet-activating factor (PAF) receptor antagonist (WEB 2086; 10 microM) reduced neutrophil adhesion. Superoxide dismutase (1,000 U/ml) had no effect. Pretreatment of HUVEC with 50 microM tungsten also blocked xanthine-induced adherence. Adhesion was also inhibited by preincubation with 100 U/ml heparin. Finally, anti-P-selectin antibody (PB1.3; 20 micrograms/ml) attenuated adhesion. Our results indicate that xanthine may promote neutrophil-endothelial adhesion via a hydrogen peroxide- and PAF-mediated P-selectin expression.
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PMID:Exogenous xanthine promotes neutrophil adherence to cultured endothelial cells. 927 12

The prerequisite for the recruitment of circulating leukocytes to sites of inflammation is adhesion to vascular endothelial cells. Selectins play a significant role in the initiation of this multistep process by mediating "rolling" of the leukocytes on the endothelium. Investigation of selectin-dependent cell interactions using function blocking monoclonal antibodies (MAb) provides insights into the mechanisms involved in leukocyte migration into inflammation. Until now most studies in inflammation models in rats have relied on cross-reactive or polyclonal antibodies against rat E-selectin. In an E-selectin knockout mouse, we aimed to generate an adhesion function blocking MAb to rat E-selectin by immunization with rat E-selectin transfected Chinese hamster ovary cells (RESEC). An IgG1 kappa MAb was identified that reacts with RESEC but not with untransfected Chinese hamster ovary cells, as well as with recombinant mouse E-selectin protein as assessed by ELISA. This MAb is designated RME-1. It does not cross-react with rat L-selectin or rat P-selectin or E-selectin expressed on human umbilical vein endothelium. Adhesion of the HL-60 myeloid cells to immobilized mouse E-selectin was completely inhibited by MAb RME-1 under static conditions and adhesion of rat polymorphonuclear leukocytes to recombinant mouse E-selectin was blocked under rotation condition. This novel antibody thus recognizes a function-related epitope on rodent E-selectin.
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PMID:Generation and characterization of a novel adhesion function blocking monoclonal antibody recognizing both rat and mouse E-selectin. 930 26

Adhesion blocking mAbs specific for rat P-, E-, and L-selectin and the alpha4-integrin were used to characterize leukocyte recruitment mechanisms in models of LTC4 (acute), LPS (subacute), and adjuvant-induced (chronic) inflammation. Intravital microscopy was employed to measure leukocyte rolling and adhesion in rat mesenteric venules. Superfusing the mesentery with 20 nM LTC4 elicited an increase in leukocyte rolling (66.8 +/- 3.8 vs 18.2 +/- 3.2 cells/min control) that was completely eliminated by an anti-rat P-selectin mAb. Superfusion with 1 microg/ml LPS induced a significant increase in leukocyte rolling within 15 min (73 +/- 8 vs 33 +/- 6 cells/min control). Rolling increased further starting at 105 min and peaked by 150 min (141 +/- 23 cells/min). LPS-induced leukocyte rolling was eliminated during the first 90 min by the P-selectin mAb. The later increase in leukocyte rolling was not prevented by a second treatment with P-selectin mAb or a function-blocking mAb against rat E-selectin. This later phase of leukocyte rolling was blocked by treatments with mAbs against either the alpha4-integrin or L-selectin. Twelve days following Mycobacterium butyricum immunization, 300 to 500 rolling cells/min were observed. This could be reduced approximately 50 to 60% by mAb against either the alpha4-integrin or L-selectin. The combination of both mAbs eliminated approximately 90% of rolling. Neither the P- nor E-selectin mAbs reduced rolling in this chronic inflammatory model. This study highlights differences in leukocyte adhesive mechanisms elicited by different stimuli and at different time points within the same vascular bed.
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PMID:Differential roles of selectins and the alpha4-integrin in acute, subacute, and chronic leukocyte recruitment in vivo. 937 52

We investigated how disruption of the actin cytoskeleton with cytochalasins modified adhesion of neutrophils rolling on a platelet monolayer in vitro at 37 degrees C. When perfused at a wall shear stress of 0.1 Pa over rolling cells, cytochalasin B, cytochalasin D and dihydro-cytochalasin B each induced dose-dependent (approximately 1-10 microg/ml) conversion to stationary attachment over minutes. Stopping was associated with cell elongation to a teardrop shape. Increased deformability of cytochalasin-treated cells was independently evidenced by more rapid entry into a micropipette. Spherical shape and rolling were reestablished concurrently on washout of the cytochalasins, while increasing the shear stress in the range 0.2 to 1.0 Pa induced tear-drop-shaped cells to restart rolling even in the continued presence of cytochalasin. When cells were pretreated with cytochalasin B, they attached efficiently at 0.1 Pa, rolled initially and only stopped after approximately 30 seconds when elongation had been established. Adhesion was selectin-mediated in the presence or absence of cytochalasin B, as judged by inhibition of attachment by antibody against P-selectin and failure of antibody against beta2-integrin CD18 to influence adhesion. Cessation of rolling is unlikely to have arisen from an increase in adhesive contact area induced by deformation because stopped cells were found to be attached only at their pointed end. Failure of adhesive bonds to peel may have arisen because selectin ligands freed of cytoskeletal restraint were dragged into this tethered region and clustered there, and because force applied to bonds was influenced by the change in cell shape. These results suggest that cytoskeletal structure is an important modulator of dynamic adhesive responses of leukocytes, via effects on adhesion receptors and cellular mechanics.
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PMID:Treatment of neutrophils with cytochalasins converts rolling to stationary adhesion on P-selectin. 942 7

Recent reports have shown that leukocyte-leukocyte adhesion is dependent on L-selectin and that leukocyte recognition of L-selectin may be mediated by P-selectin glycoprotein ligand-1 (PSGL-1). We show that the specific attachment and rolling of human neutrophils and the leukemia cell lines HL-60 and U937 on immobilized, purified L-selectin under continuous shear stress is only partially inhibited by treatment with the PSGL-1 monoclonal antibody (MoAb), KPL1 (41% to 53% inhibition), suggesting that L-selectin ligand activity in addition to PSGL-1 may mediate myeloid cell rolling on L-selectin. K562 cells cotransfected with cDNAs encoding alpha (1,3)fucosyltransferase-VII (FucT-VII) and PSGL-1 rolled on L-selectin. Adhesion of FucT-VII-PSGL-1 transfectants to L-selectin was completely blocked by MoAb KPL1, indicating that both L-selectin and P-selectin bind similar sites on PSGL-1. In support of existence of a non-PSGL-1 L-selectin ligand activity on leukocytes, an HL-60 membrane preparation immunodepleted of PSGL-1 supported rolling of L-selectin, but not P-selectin transfectants. Treatment of HL-60 cells with O-sialoglycoprotein endopeptidase inhibited attachment and rolling on L-selectin and P-selectin. However, neuraminidase treatment completely blocked HL-60 rolling on L-selectin, but not P-selectin, suggesting L-selectin and P-selectin ligand activities have different contributions of sialic acid. These findings indicate that myeloid cells express sialylated, O-linked glycoprotein ligand activity independent of PSGL-1 that supports L-selectin-mediated rolling.
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PMID:Functional characterization of L-selectin ligands on human neutrophils and leukemia cell lines: evidence for mucinlike ligand activity distinct from P-selectin glycoprotein ligand-1. 944 70

Adhesion molecule expression by pulmonary endothelial cells is considered to play an important role in the recruitment of circulating leukocytes to sites of inflammation in the lung. We have used P-selectin- and intercellular adhesion molecule type 1 (ICAM-1)-deficient mice to determine whether these adhesion molecules are important to pulmonary eosinophil recruitment after allergen challenge. There was a significant inhibition of lung tissue eosinophil recruitment in ICAM-1-deficient mice (approximately 84% inhibition compared to wild-type mice) and P-selectin-deficient mice (approximately 67% inhibition compared to wild-type mice) 3 h after allergen challenge. The number of bronchoalveolar lavage (BAL) eosinophils in P-selectin-deficient and ICAM-1-deficient mice was also significantly reduced compared with wild-type mice. Levels of BAL eosinophil peroxidase (EPO) were significantly lower in ICAM-1-deficient mice (0.21 +/- 0.03 EPO units) compared with wild-type mice (3.34 +/- 0.65 EPO units). There was no significant difference in the degree of inhibition of eosinophil recruitment in ICAM-1-deficient mice at the three time points (3, 12, and 24 h) of study after allergen challenge. However, in P-selectin-deficient mice there was a decline in the degree of inhibition of eosinophil recruitment from 3 h (67% inhibition) and 12 h (72% inhibition) postchallenge, to 24 h postchallenge (38% inhibition), suggesting that other adhesion molecules may be playing a more prominent role than P-selectin at later time points. These studies suggest an important role for ICAM-1 and P-selectin in eosinophil recruitment to the lung after allergen challenge.
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PMID:Inhibition of pulmonary eosinophilia in P-selectin- and ICAM-1-deficient mice. 947 9

Helicobacter pylori infection of the stomach results in acute inflammation followed by chronic inflammation, but the mechanism is unknown. Adhesion molecules such as ICAM-1, Mac-1, and LFA-1 may help regulate interactions of immune cells and inflammatory cells. We used immunohistochemistry to locate these molecules in the gastric mucosa of patients with chronic gastritis arising from H. pylori infection. Biopsy specimens were taken from five H. pylori-negative healthy volunteers and 20 H. pylori-positive patients with chronic gastritis for immunohistochemical studies of adhesion molecules. In the gastric mucosa of patients with H. pylori-associated chronic gastritis, ICAM-1 expression was prominent in most of the vessels and inflammatory cells, such as lymphocytes and granulocytes, in the lamina propria. However, no intraepithelial lymphocytes and surface epithelial cells expressed ICAM-1. Antigen-presenting cells (APCs), such as macrophages, expressed ICAM-1 as well as HLA-DR antigen. LFA-1 and Mac-1 were strongly expressed in these immune and inflammatory cells. The number of vascular endothelial cells positive for P-selectin was also greater in H. pylori-positive mucosa. The expression of these molecules decreased remarkably after successful eradication of H. pylori. In conclusion, ICAM-1 is the predominant form among the cell adhesion molecules that are expressed in response to chronic H. pylori infection. The increased expression of ICAM-1 is linked with massive infiltration of inflammatory cells that express LFA-1 and Mac-1, and also with APCs that express HLA-DR, suggesting that ICAM-1 exerts a key role in immuno-inflammatory responses in gastric mucosa of patients with H. pylori-associated gastritis.
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PMID:In situ expression of cell adhesion molecules in chronic gastritis with Helicobacter pylori infection. 947 51

Homeostasis is mediated through interactions of adhesion molecules on the surface of platelets which belong into the families of selectins, integrins and immunoglobulins with soluble plasma proteins, surface molecules of activated endothelial cells and molecules of extracellular matrix. The membrane expression of some adhesion molecules (P-selectin) which are the part of granular system of resting platelet identify activated platelet. Adhesion molecules of platelets could be detected by immunochemistry through flow cytometry. By this approach the inherited defects of adhesion molecules on platelets and the activated platelet could be detected. The detection of activated platelets is very useful in many clinical conditions.
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PMID:[Blood platelet adhesion molecules]. 949 Feb 6


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