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

Demonstration of murine mast cell adhesion to fibronectin (FN) following PMA-mediated cell activation raised the question whether crosslinking of high affinity IgE receptors on mouse mast cells might induce changes in adhesiveness of these cells to FN. Murine mast cells of line MCP5/L were used to investigate the effect of antigenic stimulation on cell adhesion to fN and mediator secretion. effect of antigenic stimulation on cell adhesion to FN and mediator secretion. Adhesion assays were performed using sensitized radiolabeled cells and FN- or BSA-coated 96-well plates. The presence of antigen in the concentrations up to 10 ng/ml resulted in concentration-dependent adhesion potentiation, which was detectable after 5 min, reached maximum at 30 min and persisted or decreased over the next 30 min. Adhesion potentiation decreased at antigen excess and was abolished by heat inactivation of IgE in the antiserum prior to cell treatment. External calcium ion and temperature dependence of adhesion together with the observation that RGD (Arg, Gly, Asp)--containing peptide blocked cell binding to FN suggests that FC epsilon RI crosslinking-induced adhesion potentiation involves an integrin type receptor on cell surface. Sensitized mast cells allowed to adhere spontaneously to FN released more histamine and beta-hexosaminidase upon antigen challenge. Hence, the results show the relations between IgE-induced mast cell activation, adhesion to FN and mediator secretion.
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PMID:Relations between Fc epsilon RI crosslinking-induced mast cell activation and adhesion to fibronectin. 753 25

Cytokines and adhesion molecules play a central role in the inflammatory process of respiratory allergy. Cytokines like IL4 acts on IgE synthesis and expression of low affinity CD23 IgE receptors, IL-5 on eosinophil differentiation and activation and IL-2 on T cell activation and on the expression of CD25 IL-2 receptors. IL-2, IL-4 and IL-2 soluble receptor have been studied in pollen sensitive patients before, during and after pollen season. IL-2 serum levels initially increase and decrease at the end of allergen exposition. IL-4 serum level do not significantly changes during pollen season. Adhesion molecules are essential for recruitment and migration of inflammatory cells to tissues. CD45RO T memory cells expressing generally the adhesion molecule CD29 have also been studied in a group of pollen sensitive patients. During the peak of antigen exposition CD45RO/CD29 cells significantly decrease a turnover between CD45RA naive cells and memory cells being observed. The study of cytokines and adhesion molecules could add new data on the comprehension of inflammation in respiratory allergy.
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PMID:Cytokines and adhesion molecules in respiratory allergy. 762 91

Adhesion molecules of the integrin family are implicated not only in leukocyte migration but also in leukocyte activation. Here we characterize the expression and function of fibronectin receptor integrins on rat mast cells. A rat basophilic leukemia cell line (RBL-2H3) and phorbol ester-stimulated rat peritoneal mast cells adhered to fibronectin (FN), vitronectin and fibrinogen. These mast cells expressed fibronectin receptor integrins, including very late antigen (VLA)-4, VLA-5 and vitronectin receptor (VNR), as estimated by immunofluorescent staining and inhibition of FN adherence by newly established mAbs reactive with the rat alpha 4 (MR alpha 4-1), alpha 5 (HM alpha 5-1) or beta 3 (HM beta 3-1) chains of the integrin molecules. The beta-hexosaminidase release, a marker for mast cell degranulation, triggered by high affinity IgE receptor (Fc epsilon RI)-mediated stimulation, was enhanced by adhesion of RBL-2H3 cells to either immobilized FN, MR alpha 4-1, HM alpha 5-1 or HM beta 3-1. This FN enhancement of beta-hexosaminidase release was inhibited by soluble MR alpha 4-1, HM alpha 5-1 and HM beta 3-1 as well as by GRGDSP and DELPQLVTLPHPNHLGPEILDVPST peptides which abrogate VLA-5/VNR and VLA-4 binding to FN respectively. In vivo, passive cutaneous anaphylaxis induced by IgE anti-DNP and DNP-BSA was inhibited by concurrent s.c. injection of MR alpha 4-1, HM alpha 5-1 and HM beta 3-1. These results demonstrate that FN receptor integrins expressed on rat mast cells play an important role in regulating mast cell activation both in vitro and in vivo.
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PMID:Expression and function of fibronectin binding integrins on rat mast cells. 773 20

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

The aim of this work is to contribute to increasing our knowledge of asthma. The IgE can't alone be imputed in the anaphylactic reaction. Asthma is a bronchial inflammatory disease. The secretion of lymphokines increases the inflammatory response. The eosinophils cells damage the respiratory epithelium. The mast cells and the basophils cells release the chemical mediators and also the cytokines. The adhesion molecules situated in the cell membrane permit leukocyte cells to integrate with extracellular matrix during intra-tissue migration. Adhesion molecules may play a primary role in the pathogenesis of inflammatory response. The key role of the CD4 + T lymphocytes subset appeared in the last years.
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PMID:[From IgE to the cell adhesion molecule]. 777 45

The physiological function of many cells is dependent on their ability to adhere via receptors to ligand-coated surfaces under fluid flow. We have developed a model experimental system to measure cell adhesion as a function of cell and surface chemistry and fluid flow. Using a parallel-plate flow chamber, we measured the binding of rat basophilic leukemia cells preincubated with anti-dinitrophenol IgE antibody to polyacrylamide gels covalently derivatized with 2,4-dinitrophenol. The rat basophilic leukemia cells' binding behavior is binary: cells are either adherent or continue to travel at their hydrodynamic velocity, and the transition between these two states is abrupt. The spatial location of adherent cells shows cells can adhere many cell diameters down the length of the gel, suggesting that adhesion is a probabilistic process. The majority of experiments were performed in the excess ligand limit in which adhesion depends strongly on the number of receptors but weakly on ligand density. Only 5-fold changes in IgE surface density or in shear rate were necessary to change adhesion from complete to indistinguishable from negative control. Adhesion showed a hyperbolic dependence on shear rate. By performing experiments with two IgE-antigen configurations in which the kinetic rates of receptor-ligand binding are different, we demonstrate that the forward rate of reaction of the receptor-ligand pair is more important than its thermodynamic affinity in the regulation of binding under hydrodynamic flow. In fact, adhesion increases with increasing receptor-ligand reaction rate or decreasing shear rate, and scales with a single dimensionless parameter which compares the relative rates of reaction to fluid shear.
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PMID:Receptor-mediated binding of IgE-sensitized rat basophilic leukemia cells to antigen-coated substrates under hydrodynamic flow. 803 94

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

Rat basophilic leukemia cells will adhere to and spread out on fibronectin coated surfaces in an integrin dependent manner. Adhesion and spreading on fibronectin leads to increased degranulation, inositol phosphate production, phospholipase D activation, and increased production of prostaglandin D2 and leukotriene C4 when the cells are activated through the high affinity IgE receptor. Rat basophilic leukemia cells will also adhere to surfaces coated with anti-rat class I antibodies, poly-L-lysine, and a lectin purified from Tetragonolobus purpureas. In all cases, antigen activated cells, which were adherent, displayed increased signaling, degranulation and eicosanoid production as compared to cells which were non-adherent. Cells which adhere to either anti-rat class I antibodies or poly-L-lysine also spread even though this is not mediated through integrins. In contrast, adhesion to the lectin from Tetragonolobus did not cause any appreciable spreading unless the cells were also triggered through the IgE receptor. Cells were also able to bind to fibronectin immobilized on polystyrene beads which mimics adhesion but does not allow spreading. However, these cells exhibited no increased signaling, degranulation, or eicosanoid production. Furthermore, rat basophilic leukemia cells can be modified by incubating them in the presence of biotinylated-phosphatidylserine which becomes incorporated into the membrane. These modified cells will adhere to streptavidin coated plates while unmodified cells will not. However, these modified cells do not spread, even after activation with antigen, and they show no increased degranulation or production of eicosanoids. These results indicate that adhesion itself is not sufficient for upregulation of the cells in response to antigen and that spreading of the cells may be the critical component.
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PMID:Increased degranulation and phospholipase A2, C, and D activity in RBL cells stimulated through FcepsilonR1 is due to spreading and not simply adhesion. 909 51

Antigen-antibody systems provide the flexibility of varying the kinetics and affinity of molecular interaction and studying the resulting effect on adhesion. In a parallel-plate flow chamber, we measured the extent and rate of adhesion of rat basophilic leukemia cells preincubated with anti-dinitrophenyl IgE clones SPE-7 or H1 26. 82 to dinitrophenyl-coated polyacrylamide gel substrates in a linear shear field. Both of these IgEs bind dinitrophenyl, but H1 26.82 has a 10-fold greater on rate and a 30-fold greater affinity. Adhesion was found to be binary; cells either arrested irreversibly or continued at their unencumbered hydrodynamic velocity. Under identical conditions, more adhesion was seen with the higher affinity (higher on rate) IgE clone. At some shear rates, adhesion was robust with H1 26.82, but negligible with SPE-7. Reduction in receptor number or ligand density reduced the maximum level of adhesion seen at any shear rate, but did not decrease the shear rate at which adhesion was first observed. The spatial pattern of adhesion for both IgE clones is well represented by the first-order kinetic rate constant kad, and we have determined how kad depends on ligand and receptor densities and shear rate. The rate constant kad found with H1 26.82 was approximately fivefold greater than with SPE-7. The dependence of kad on site density and shear rate for SPE-7 is complex: kad increases linearly with antigen site density at low to moderate shear rates, but is insensitive to site density at high shear. kad increases with shear rate at low site density but decreases with shear at high site density. With H1 26.82, the functional dependence of kad with shear rate was similar. Although these data are consistent with the hypothesis that we have sampled both transport and reaction-limited adhesion regimes, they point out deficiencies in current theories describing cell attachment under flow.
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PMID:Kinetics of adhesion of IgE-sensitized rat basophilic leukemia cells to surface-immobilized antigen in Couette flow. 978 56

Mast cells are involved in both the genesis of allergic inflammation and in host defense; and reside in tissues where their location and responsiveness is regulated in part by adhesion to extracellular matrix proteins (ECM). We have reported that human mast cells (huMC) express TLR1-7, and 9 and respond to toll-like receptors (TLR) ligands by releasing cytokines and leukotriene C4. To determine if TLR ligation could similarly affect mast cells via an influence on adhesion, we employed huMC; and as substrates, fibronectin (FN) and vitronectin (VN). huMC were thus treated with double-stranded RNA (dsRNA) and adhesion to ECM was quantified. FcvarepsilonRI dependent mast cell degranulation was assessed. Adhesion molecule expression and activation was measured by flow cytometry. Activation of huMC through TLR3 with increasing amounts of polyI:C inhibited mast cell adhesion in a dose-dependent manner. This decrease in adhesion was accompanied by a similar decrease in IgE-mediated mast cell degranulation. Activation of TLR3 on huMC resulted in a change in the conformation of CD29, the receptor for FN, to an inactive form. Thus, TLR3 activation decreases mast cell attachment to VN and FN through an active process and one, which would abrogate mast cell attachment dependent potentiation of IgE-mediated responses.
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PMID:TLR3 activation inhibits human mast cell attachment to fibronectin and vitronectin. 1628 Jan 66


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