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

The ability of rabbit alveolar macrophages to specifically recognize and adhere to surfaces derivatized with carbohydrates was examined. Otherwise inert polyacrylamide gels were derivatized with aminohexylglycosides as previously described (Guarnaccia, S. P., and Schnaar, R. L. (1982) J. Biol. Chem. 257, 14288-14292). Intact viable rabbit alveolar macrophages, isolated by lung lavage, were placed in contact with surfaces derivatized with different glycosides. Only those surfaces derivatized with alpha-D-mannose residues were capable of supporting rabbit alveolar macrophage adhesion. Adhesion was rapid, obtaining maximal levels within 10 min, and occurred readily at either 0 or 37 degrees C. The carbohydrate specificity of the cell adhesion was investigated by the use of soluble carbohydrate inhibitors. The potency of various saccharides to block the adhesion correlated with that demonstrated for blocking the uptake or binding of radiolabeled soluble glycoproteins (Shepherd, V. L., Lee, Y. C., Schlesinger, P. H., and Stahl, P. D. (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 1019-1022). Thus, the order of potency observed was: D-Man congruent to L-Fuc greater than D-GlcNAc congruent to D-Glc much greater than D-Gal congruent to D-GalNAc congruent to L-rhamnose. While soluble monosaccharides were capable of blocking adhesion when added in millimolar concentrations, polymannosylated neoglycoproteins were able to block adhesion in the nanomolar concentration range. Adhesion to the mannose-derivatized surfaces was a dynamic event even at 0 degrees C, since adhesion was less susceptible to monosaccharide inhibition at later incubation times. Surfaces derivatized with aminohexyl S-mannoside ligands were more effective in supporting adhesion than those derivatized with the corresponding O-mannosides. Soluble inhibitor studies suggest that this was due to a more favorable conformation of the S-glycoside for binding to the cell surface receptor. The results reported here demonstrate that the previously reported alveolar macrophage mannose/fucose receptor can mediate carbohydrate-specific cell adhesion.
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PMID:Carbohydrate-specific adhesion of alveolar macrophages to mannose-derivatized surfaces. 669 35

The present work concerned the study of the sub-minimal inhibitory doses of tetracyclin, doxycyclin and minocyclin on both hemagglutinating activity and adhesion capacity demonstrated in three E. coli strains isolated from urine. Two different types of hemagglutinins, mannose-resistant (HAMR) and mannose-sensitive (HAMS), were associated in two strains; HAMR was present in the third strain. Adhesion capacity was detected, in vitro, with uroepithelial cells spontaneously eliminated in urine. Whatever the antibiotic used, HAMR titers clearly decreased. In contrast, the effect of these antibiotics on the HAMS titers was inconstant, according to the bacterial strain or the antibiotic used. Adhesion capacity was inhibited particularly in the presence of tetracyclin and doxycyclin. Minocyclin was not a very good inhibitor molecule. The analysis of coefficient of correlation showed that the ability of adhering to uroepithelial cells was related to the HA titers. But it is impossible to say if the same bacterial structure migt be considered as mediator for both HA and adhesion capacity.
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PMID:[Haemagglutinins and adhesins of Escherichia coli strains isolated from urine: inhibitory effect of sub-inhibitory concentrations of tetracycline, doxycycline and minocycline. Preliminary results ]. 675 May 23

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 occurrence of recurrent bacterial infections, neutrophil motility dysfunction and normal expression of beta 2 integrins (CD18) in two unrelated children suggested an as yet undescribed adhesion deficiency. The fact that both children exhibited the rare Bombay blood group and were Lewis negative, each involving carbohydrates with different fucose linkages, suggested a possible defect in the fucose-containing ligand for E- and P-selectin, sialyl Lewis X (SLe(x)). Using a monoclonal anti-SLe(x) antibody, we did not detect expression of SLe(x) on the neutrophils of the patients. Adhesion of neutrophils to endothelial cells activated with interleukin-1 beta or histamine was markedly decreased ( < 5% of control). The observation that the neutrophils did not bind to recombinant E-selectin and purified P-selectin confirmed the SLe(x) deficiency as the basis for adhesion deficiency. Using several in vivo techniques, we were able to show that neutrophil rolling, the first step in their adhesion, is markedly decreased, and therefore neutrophil emigration through the endothelium and arrival at site of inflammation is significantly diminished (1-2% of normal). Low binding of fucose-specific lectins to the patients' B lymphocytes transformed with Epstein-Barr virus was observed, while the binding of mannose-specific lectins was normal, providing further evidence for a general fucose deficiency as the primary defect. The existence of the patients and their deficiency emphasizes the essential role of the endothelial cell selectins and their ligand, SLe(x), in recruitment of neutrophils to sites of infection.
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PMID:Leukocyte adhesion deficiency (LAD) II. 758 37

We have shown previously that rat liver macrophages (Kupffer cells) express a membrane-bound form of C-reactive protein (mCRP) on their surface which is identical to a galactose-specific particle receptor activity. We now establish the presence of mCRP on human monocyte-macrophages using immunocytochemistry with an anti-neoCRP specific monoclonal antibody and RNA-RNA in situ hybridization to demonstrate the presence of CRP-specific mRNA. Concomitant with mCRP expression, cells exhibit galactose-dependent uptake of particles coated with lactosylated bovine serum albumin. Adhesion experiments on fibronectin-coated surfaces that mCRP on human blood monocytes may act as a selectin-like adhesion molecule, mediating initial carbohydrate-specific contacts which are followed by peptide-specific recognition via integrin receptors.
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PMID:Expression of membrane-associated C-reactive protein by human monocytes: indications for a selectin-like activity participating in adhesion. 762 Mar 28

Using electron microscopy and cytofluorimetry we studied the role of carbohydrate-specific recognition systems in the interaction of apoptotic bodies with normal and interleukin 1-activated sinusoidal endothelial cells. Microfluorimetric observation of liver tissue sections revealed octadecylrhodamine B-labelled apoptotic body binding to the sinusoidal wall of mouse liver, when they were injected intraportally. Plate-scanning cytofluorimetry demonstrated that about 20-25% of Acridine Orange-labelled apoptotic bodies could adhere specifically to cultured endothelial cells after 15 minutes of incubation. Adhesion increased to 30% when the cells were incubated for 60 minutes. Using a mixture of galactose/N-acetylglucosamine/mannose as competition solution apoptotic body adhesion was significantly reduced especially after longer times of incubation, when the percentage of inhibition reached 50%. Following 4 hours exposure of liver endothelial cells to 1 ng/ml human recombinant interleukin-1 beta adhesion markedly increased after 60 minutes of incubation, whereas the co-incubation of interleukin-1 beta with the inhibitors brings down the adhesion to basal values obtained in controls. Electron microscopic observation of the adhesion process showed that the number of endothelial cells binding apoptotic bodies gradually increased from low to high values with time. After 60 minutes of incubation, the majority of apoptotic bodies were seen inside phagosomes and only a few remained at the cell surface. Liver endothelial cells bound and endocytosed apoptotic bodies through carbohydrate-specific receptors. Moreover, this scavenger action was interleukin-1 enhanced, thus suggesting its possible activation during inflammatory and immune processes.
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PMID:Phagocytosis of apoptotic bodies by liver endothelial cells. 762 23

One hundred and one strains of enterotoxemic Escherichia coli (ETEEC) O-group 139 isolated from swine with edema disease were investigated for their adherence to HEp-2 cells in the presence of D-mannose. All strains adhered in large numbers to the cells (21 to 60 bacteria/cell). No correlation was found between the presence of F107 fimbria on the organisms and the adherence to the cells. Adhesion-inhibition tests showed that anti-K12 serum inhibited the adhesion ETEEC O-group 139 (an inhibition rate of 63 to 65%), but anti-F107 or anti-O139 sera did not. These results indicate that the capsular K12 antigen may be one of the pathogenic factors of ETEEC O-group 139.
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PMID:[Adherence to HEp-2 cells of enterotoxemic Escherichia coli O-group 139 from pigs with edema disease]. 762 22

Twelve haemagglutinating and non-haemagglutinating isolates of Aeromonas spp., comprising 6 each of clinical and environmental origin, were examined for their ability to adhere to rabbit intestinal epithelium, for inhibition of adhesion with sugars, and for delineation of the portion of intestine, jejunum, or ileum that is most susceptible to adhesion. Although the environmental isolates of Aeromonas haemagglutinated human erythrocytes that were inhibited by D-mannose and/or L-fucose, the majority of the clinical isolates of Aeromonas adhered to rabbit intestinal epithelium in almost equal proportions regardless of their haemagglutination (HA) properties, species designation, and source of isolation. Adhesion of both haemagglutinating and non-haemagglutinating isolates of Aeromonas was inhibited by sugars; however, the ability of sugar inhibition to adhere was similar to that observed with HA. This study suggests that adhesion is probably mediated by a variety of pilus or non-pilus colonisation factors which may or may not be a haemagglutinin. The jejunum was found to be more susceptible to adhesion than the ileum. However, no appreciable difference was observed in the number of adhered bacteria to adjacent loops.
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PMID:Adherence of haemagglutinating and non-haemagglutinating clinical and environmental isolates of Aeromonas. 826 4

The enteropathogenicity of Aeromonas strains that showed mannose-resistant adhesion to INT407 cells was evaluated by infecting Caco-2 cells and observing them by light and electronmicroscopy. Five of six strains adhered in large numbers to Caco-2 cells in the presence of mannose and caused cytopathic effects. Two strains of Aeromonas spp. seemed to invade Caco-2 cells, as membrane-bound bacteria were seen within the cytoplasm of these cells; however, staining by acridine orange-crystal violet appeared to show intracellular fluorescent bacteria in three strains. Fimbriae did not appear to play an important role in adhesion because fimbrial structures were not seen by transmission electronmicroscopy. Adhesion of four strains was inhibited by the addition of L-fucose. The strains were negative in the fluorescence actin staining test, which in enteropathogenic Escherichia coli strains correlates with the ability to attach and efface intestinal microvilli. The DNA of the Aeromonas strains did not hybridise with the E. coli eae and ipaB probes, associated with attaching and effacing ability and invasion, respectively. These results give support to the enteropathogenicity of adhesive strains of Aeromonas spp., although the mechanisms of adhesion, and possibly invasion, remain to be elucidated.
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PMID:Adhesion to and invasion of human colon carcinoma Caco-2 cells by Aeromonas strains. 828 15

The purpose of this study was to identify components of saliva that interact with Candida albicans in solution and that may modulate adhesion to dental acrylic (polymethylmethacrylate [PMMA]) surfaces. Saliva-derived pellicles extracted from C. albicans blastoconidia and hyphal-form cells mixed with fresh human submandibular-sublingual saliva (HSMSL) contained predominantly high- and low-molecular-weight mucins (MG1 and MG2, respectively). In contrast, few components from fresh human parotid saliva were adsorbed to yeast cells. Coating PMMA beads with HSMSL significantly enhanced (10-fold) adhesion of both growth forms of C. albicans compared with human parotid saliva (2-fold), suggesting a role for mucins in adhesion. HSMSL-enhanced adhesion was completely abolished by preadsorbing HSMSL with either blastoconidia or hyphal-form cells prior to coating PMMA. However, coating PMMA with purified salivary mucins or the addition of mucin to preadsorbed saliva did not enhance or restore adhesion to levels found with fresh HSMSL. Adhesion assays employing guanidine-treated fresh HSMSL showed a complete lack of Candida binding, suggesting that subjecting HSMSL to dissociating conditions may alter a property of salivary mucins crucial for C. albicans adhesion. Protease and glycosidase treatment of yeast cells significantly reduced adhesion to HSMSL-coated PMMA. In addition, preincubation of C. albicans with mannose and galactose inhibited adhesion to HSMSL-coated PMMA. These results suggest that mucins may play a role in C. albicans adhesion to saliva-coated PMMA and that a glycoprotein on the yeast surface may be involved in these events.
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PMID:Human submandibular-sublingual saliva promotes adhesion of Candida albicans to polymethylmethacrylate. 850 Sep 3


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