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

Adhesion of baby hamster kidney fibroblasts (BHK cells) to a Falcon tissue culture flask was measured under various physiological conditions. While 75-80% of the fibroblasts adhere at temperatures from 19-50 degrees, cellular adhesion decreased dramatically below 19 degrees. Less than 10% of the cells adhere to the substratum even after prolonged incubations at temperatures of 8 degrees or below. This lack of adhesion at low temperatures cannot be overcome by the application of increased gravitational force to the cells. No correlation exists between cellular ATP concentrations or respiration rates and the rate of cell adhesion to the substratum. One millimolar Na F and 1 mM 2,4 dinitrophenol together lower cellular ATP concentration by 95% but adhesion is reduced by only 50%. NaN3 and KCN greatly lower cellular ATP concentrations without a corresponding inhibition of adhesion. Inhibition of cellular respiration by these compounds occurs at lower concentrations than does the inhibition of adhesion. Two micrograms/milliliters of cytochalasin B inhibits adhesion by 90%, 0.1 mM vinblastine sulphate or colchicine by less than 50% and 50 microgram/ml colcemid by less than 30%. Fixing the cells with formaldehyde, hardening their membranes with ZnCl2 or treating the cells with toluene, all cause an inhibition in adhesion. Again, application of increased gravitational force cannot overcome these latter inhibitions of BHK cell adhesion to the surface of the flasks.
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PMID:Effects of temperature, metabolic and cytoskeletal inhibitors on the rate of BHK cell adhesion to polystyrene. 56 Oct 77

The presence of pericardial adhesions may increase morbidity and mortality during reoperation for cardiac disease. Pericardial substitutes (patches) are commercially available, and reportedly they reduce or prevent adhesions. We implanted five (1984 to 1985) newer pericardial substitutes in dogs. A new polytetrafluoroethylene surgical membrane, two types of glutaraldehyde-stabilized bovine pericardium, formaldehyde-preserved bovine pericardium, and glutaraldehyde-stabilized equine pericardial patches were each implanted in six adult dogs (total 30 dogs) with two dogs from each of the five groups killed at 3, 9, and 18 months. At autopsy the condition of each patch was recorded photographically, and specimens were substituted for histologic examination. Adhesions and epicardial reactions were graded as none, minimal, moderate, or severe. None of the materials produced severe pericardial adhesions, and no adhesions were detected in nine dogs. Eleven dogs had no epicardial reaction and only one showed a severe reaction. Adhesions to portions of the suture line required sharp dissection in 11 dogs. If there is concern over the possibility of calcification in heterologous tissue, polytetrafluoroethylene may be chosen. Patch type did not significantly alter patch behavior.
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PMID:A new look at pericardial substitutes. 361 29

Escherichia coli strain S5 (O15:K+:H21) isolated from a septicaemic lamb and previously shown to possess a virulence plasmid, Vir, attached in vitro to calf epithelial tissue from the ileum, oesophagus and trachea in the presence of 0.5% (w/v) D-mannose. The Vir+ recombinant strains 711v and H209av, which had received the Vir plasmid(s) from strain S5, also attached to these epithelia but the parent strains 711 and H209a without the Vir plasmid were non-adhesive. The attachment of the Vir+ strain 711v to intestinal brush borders was inhibited by antiserum to live Vir+ strain H209av but not by antiserum to strain H209a lacking Vir. No adherence occurred with Vir+ organisms grown at 18 degrees C or after heating at 65 degrees C. Adhesion was unaffected by 0.5% (w/v) formaldehyde. Glucosamine, mannosamine, their N-acetyl derivatives and wheat germ lectin each inhibited attachment of Vir+ strain 711v to brush border epithelia.
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PMID:Adhesive properties associated with the Vir plasmid: a transmissible pathogenic characteristic associated with strains of invasive Escherichia coli. 675 81

The adherence of Yersinia pseudotuberculosis to the surface of HeLa cells at 4 degrees C was studied. This temperature allows adhesion of bacteria but prevents engulfment. Adhesion between the bacteria and the cells was not dependent upon the presence of serum, Ca2+ or Mg2+ in the medium. Maximum adhesion was obtained at pH 6.5-7.9 and pretreatment of the cells with formaldehyde or glutaraldehyde inhibited the attachment of the bacteria. The interaction between the bacteria and the cell surface seems to involve cellular processes that are mostly microvilli. An intimate association between the bacteria and the cellular glycocalyx was found. Three virulent bacterial strains adhered more easily to the cell surface than five avirulent strains. Maximum adherence was obtained with bacteria from late logarithmic and early stationary phases of growth. The bacteria gradually lose their adhesive property when cultivated for several generations at 37 degrees C in nutrient broth but not when cultivated at 20 degrees C. Treatment of the bacteria with protease IV from Streptomyces caespitosus markedly reduced the efficiency of attachment.
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PMID:Interaction between Yersinia pseudotuberculosis and the HeLa cell surface. 687 36

Multiple, linked interactions between the platelet surface and collagen fibers have been implicated in the initiation of platelet secretion and subsequent aggregation. The formation of such multiple simultaneous interactions could give rise to high affinity adhesion of platelets to collagen even though the affinity of the individual interactions may be much weaker. This concept has been tested by measuring the adhesion of platelets to collagen under conditions which could effect the formation of multiple interactions. Adhesion is markedly diminished at 4 degrees C but not at 23 or 37 degrees C. Metabolic inhibitors such as 2-deoxyglucose and Antimycin A do not inhibit adhesion although they virtually abolish subsequent aggregation. Brief formaldehyde fixation of platelets greatly reduces adhesion. These results are consistent with the concept that the formation of multiple linked interactions between the platelet surface and collagen are important in platelet-collagen adhesion and that mobility of platelet membrane components is required for the clustering of these interactions in focussed regions on the platelet surface.
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PMID:Platelet-collagen adhesion-membrane fluidity and the development of high affinity adhesion through multiple interacting sites. 734 33

Adhesion of parasitized red blood cells to vascular endothelium contributes to the ischaemic pathology of severe falciparum malaria. One of the endothelial cytoadhesion receptors, CD36, is also expressed by platelets. We have studied adhesion of flowing parasitized cells to a surface coated with immobilized, activated platelets, both as a model for CD36-mediated adhesion and because interaction with platelets might play a direct role in thrombotic complications of malaria. Parasitized cells were able to bind firmly to platelets over a range of shear stress (up to 0.3 Pa) close to those found in the microcirculation. The binding was largely abolished by treatment of platelets with antibody to CD36, with only a small effect by antibody to ICAM-1. Binding showed pH sensitivity consistent with previous reports of CD36-mediated cytoadhesion. Fixation of the platelet surface with formaldehyde preserved adhesion and its antibody sensitivity, while fixation with glutaraldehyde greatly reduced adhesion and increased the sensitivity to antibody against ICAM-1. Thus CD36-mediated binding is inhibited by glutaraldehyde--but not formaldehyde--fixation, while ICAM-1 can mediate adhesion after either form of fixation. We conclude that platelet-coated surfaces (with or without fixation) represent a practically simple model for studying malarial cytoadhesion and that platelets are likely to be able to bind parasitized cells in vivo and could thus promote vascular occlusion.
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PMID:Plasmodium falciparum: characterization of adhesion of flowing parasitized red blood cells to platelets. 752 16

Adhesion of parasitized red blood cells to vascular endothelium is considered to be a major factor in the pathophysiology of falciparum malaria, and so the molecular mechanisms and rheologic characteristics of this interaction are of profound importance. We have investigated the adhesive behavior of wild-type parasite isolates cultured from the blood of Gambian children with falciparum malaria and allowed to flow over surfaces coated with formaldehyde-fixed human umbilical vein endothelial cells (HUVEC) or platelets. Parasitized cells were able to attach to HUVEC and/or to platelets, and studies with monoclonal antibodies showed that intercellular adhesion molecule-1 (ICAM-1) and CD36 antigen were the major mediators of adhesion for the two surfaces, respectively. The levels of adhesion to HUVEC and to platelets were highly variable but did not correlate with each other, so that different isolates express independently variable capacities to bind to the two receptors. Adhesion was stationary for platelets and generally at a higher level compared with binding to HUVEC, which was predominantly (about 60%) of a rolling type. The stationary component of adhesion to HUVEC represented a greater proportion of adhesion for the wild isolates than for laboratory-adapted strains, and this form of adhesion was relatively insensitive to antibody to ICAM-1. This suggests the existence of an additional endothelial cell-expressed receptor for the wild isolates. These studies show wide variation in the ability of wild isolates of Plasmodium falciparum to adhere to ICAM-1, CD36 antigen, and possibly other receptors in the presence of physiologically relevant flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of cytoadhesion of flowing, parasitized red blood cells from Gambian children with falciparum malaria. 754 44

Human umbilical vein endothelial cells (HUVEC) were used as an experimental host model to investigate the mechanism(s) of streptococcal adhesion in infective endocarditis. Adhesion activity of Streptococcus gordonii was maximal during the logarithmic phase of growth and was greatly reduced or eliminated by pretreatment of bacteria with heat, formaldehyde, or trypsin. At saturating numbers of streptococci, an average of 81 bacteria were bound per HUVEC. Streptococcal adhesion was inhibited by low-molecular-weight dextran and heparin but not by sucrose, fibronectin, or laminin. Adhesion was also prevented by pretreatment of HUVEC with proteins dissociated from the surface of S. gordonii with 10 mM EDTA or isolated from spent culture medium. Western blot (immunoblot) assays detected a single adhesion protein of 153 kDa (AP153) on HUVEC after incubation with unfractionated extracts of streptococci. The adhesin exhibited glucosyltransferase (GTF) activity when incubated with sucrose and Triton X-100 after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The AP153 was purified by affinity chromatography on dextran beads and show to have binding activity for HUVEC, GTF activity, an amino acid composition similar to that reported for GTF of S. gordonii, and the ability to inhibit S. gordonii adhesion. Incubation of the streptococci with antibodies to the adhesin inhibited bacterial attachment to HUVEC monolayers. These results indicate that surface-localized GTF mediates adhesion of S. gordonii to HUVEC in vitro and may serve as a mechanism for colonization of the endocardium in infective endocarditis.
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PMID:Glucosyltransferase mediates adhesion of Streptococcus gordonii to human endothelial cells in vitro. 818 39

We have extended our previous studies of adherent neutrophils and compared actin depolymerization and intracellular calcium changes induced by adherence to laminin and fibronectin. In order to accurately assess cellular actin changes, F-actin depolymerization in the cell lysates must be inhibited. We found that phalloidin or 3.7% formaldehyde treatment effectively inhibited the depolymerization of F-actin fragments following cell lysis. Formaldehyde and phalloidin treatment reduced G-actin levels 75-80% in suspended cells, 35-73% in cells adherent for 1 min, and about 50% for cells adherent for 3 min. When the actin was fixed, there were highly significant differences in G-actin levels between the suspended and adherent cells as compared with unfixed cells. Adhesion to both laminin and fibronectin initiated a rapid rise in G-actin with a corresponding decrease in F-actin. However, the changes were more pronounced in cells adherent to laminin. The peak of depolymerization occurred by 1 min and, thereafter, G-actin decreased and F-actin increased reaching a steady state at 5 min. Adhesion to both laminin- and fibronectin-coated surfaces was accompanied by an increase of [Ca2+]i with a peak at 3 min, followed by a decrease from 3-5 min and a steady state attained between 5 and 10 min. The rise of [Ca2+]i in laminin-adherent cells was about twice that in fibronectin-adherent cells at 3 min (P < 0.02). Pertussis toxin, H-7, and staurosporin treatments did not alter the dynamic changes of actin in adherent cells, suggesting that these metabolic events are transduced by a G-protein and Protein Kinase C independent mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assembly dynamics of actin in adherent human neutrophils. 829 48

Normal circulating platelets do not adhere to intact, undisturbed endothelium. Studies have shown, however, that platelets will adhere to virally infected or thrombin-stimulated human umbilical vein endothelial cells. Using a novel platelet/endothelial cell adhesion assay we studied the interaction of thrombin-activated platelets to human saphenous vein endothelial cells (HSVEC), and its mechanism(s). Biotinylated platelets were exposed to Hepes-Tyrode buffer, 10E5 or PAC-1 [monoclonal antibodies (Mabs) blocking GPIIb-IIIa], AK4 (Mab blocking P-selectin, 6D1 (Mab blocking vWf binding to GPIb), RGDS (small peptide blocking the fibrinogen binding site), or EDTA (dissociates GPIIb-IIIa complex) and then activated with thrombin. The platelets were subsequently exposed to thrombin-stimulated monolayer HSVEC. Phycoerythrin-streptavidin was added to the wells to fluorescently label the platelets, followed by formaldehyde fixation and washing to remove nonadherent platelets. Adhesion of platelets to HSVEC was assessed using a fluorescent multiwell plate reader. Antibodies which blocked the GPIIb-IIIa receptor and agents which competitively bound the receptor all significantly inhibited activated platelet adhesion to the activated HSVEC. We have found that thrombin significantly increases platelet/HSVEC adhesion, and this event is mediated via the integrin GPIIb-IIIa (fibrinogen receptor). These GPIIb-IIIa receptor blocking Mabs and RGDS may be useful adjuncts for improving patency following angiographic intervention and/or vein grafting in patients with high risk of thrombosis. The assay we have developed is a valuable and relatively simple method for assessing platelet/endothelial cell adhesion and activation.
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PMID:Adhesion of activated platelets to venous endothelial cells is mediated via GPIIb/IIIa. 865 40


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