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

This thesis is based on 8 publications and a review of the literature. The aim was to summarize present knowledge on molecular components of Yersinia enterocolitica involved in (i) adhesion, with special reference to plasmid encoded factors and (ii) induction of antibodies in the host, and the quantitation of these two phenomena. Adhesion of Y. enterocolitica was quantitatively studied by methods that measured binding to cultured epithelial cells, mucosal constituents immobilized on polystyrene, intestinal tissue, and nonbiological solid surfaces. The chromosomal inv and ail gene products have been shown by others to be independently able to mediate adhesion to and invasion of cultured epithelial cells. However, the Yersinia virulence plasmid, pYV, also encodes for at least one product that may mediate adhesion. It was shown that pYV carrying Y. enterocolitica strains adhered more efficiently than their isogenic pYV cured derivatives to rabbit and human ileal intestinal tissue and to rabbit ileal brush border membrane vesicles (BBVs). Using Y. enterocolitica mutants that were defective for production of the pYV encoded outer membrane protein, YadA, and Escherichia coli strains carrying the cloned yadA gene it was verified that YadA was responsible for the pYV encoded adhesion. The YadA promoted adhesion was found likely to be non-specific and, at least in part, mediated by hydrophobic interaction. YadA, however, also mediated binding to one or more constituents present in intestinal mucus. Such binding led to decreased ability to penetrate a layer of mucus in vitro and subsequent decreased ability to adhere to BBVs. Based upon these results, it remains uncertain whether Y. enterocolitica is able to benefit from the YadA mediated adhesion in the intestinal millieu. In vivo results have suggested that expression of YadA confers on Y. enterocolitica an increased ability to colonize the intestine, but no definitive conclusions have been reached so far. A large number of antigens were identified in Y. enterocolitica by means of crossed immunoelectrophoresis (XIE). Quantitation of serological cross-reactions between chromosome-encoded Y. enterocolitica antigens and antigens from other bacterial species was performed by means of XIE and proved useful for taxonomic purposes. Using XIE it was shown that infection with Y. enterocolitica induced an antibody response against a wide range of antigens. Tube agglutination, enzyme linked immunosorbent assays (ELISAs) using purified lipopolysaccharide (LPS) or formalin-killed whole pYV carrying cells as antigens, and XIE were evaluated for their applicability to detect recent Y. enterocolitica O:3 infection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions between Yersinia enterocolitica and the host with special reference to virulence plasmid encoded adhesion and humoral immunity. 161 21

An enzyme-linked immunosorbent assay system was developed and used to study adhesion of Pseudomonas aeruginosa to human epithelial cells and the abilities of specific antibodies to inhibit this process. Human buccal epithelial cells coated onto microtiter plates were incubated with P. aeruginosa suspensions, and adherent bacteria were detected by using anti-P. aeruginosa serum and a horseradish peroxidase-conjugated secondary antiserum. Adhesion, quantitated as an increase in A405, varied linearly with increasing numbers of bacterial CFU added per well in the range of 10(5) to 10(8) CFU per well. Adhesion of P. aeruginosa increased following trypsinization of buccal epithelial cells. Preincubation of bacteria with monoclonal antibodies directed against P. aeruginosa outer membrane protein H2 inhibited adhesion with all eight of the isolates tested. Preincubation of P. aeruginosa with sera from infected cystic fibrosis patients also resulted in inhibition of adhesion in the enzyme-linked immunosorbent assay system. This inhibitory activity was shown to be due to two factors: P. aeruginosa-specific immunoglobulin G and a non-immunoglobulin G serum component. These data support the hypothesis that bacterial components other than pili are involved in adhesion and suggest that anti-P. aeruginosa antibodies may be of use in preventing adhesion and subsequent colonization with P. aeruginosa.
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PMID:Characterization of antibody-mediated inhibition of Pseudomonas aeruginosa adhesion to epithelial cells. 163 1

The initial step in extravasation of neutrophils (polymorphonuclear leukocytes [PMNs]) to the extravascular space is adherence to the endothelium. We examined the effect of oxidants on this process by treating human endothelial cells with H2O2, t-butylhydroperoxide, or menadione. This resulted in a surface adhesive for PMN between 1 and 4 h after exposure. The oxidants needed to be present only for a brief period at the initiation of the assay. Adhesion was an endothelial cell-dependent process that did not require an active response from the PMN. The adhesive molecule was not platelet-activating factor, which mediates PMN adherence when endothelial cells are briefly exposed to higher concentrations of H2O2 (Lewis, M. S., R. E. Whatley, P. Cain, T. M. McIntyre, S. M. Prescott, and G. A. Zimmerman. 1988. J. Clin. Invest. 82:2045-2055), nor was it ELAM-1, an adhesive glycoprotein induced by cytokines. Oxidant-induced adhesion did not require protein synthesis, was inhibited by antioxidants, and, when peroxides were the oxidants, was inhibited by intracellular iron chelators. Granule membrane protein-140 (GMP-140) is a membrane-associated glycoprotein that can be translocated from its intracellular storage pool to the surface of endothelial cells where it acts as a ligand for PMN adhesion (Geng, J.-G., M. P. Bevilacqua, K. L. Moore, T. M. McIntyre, S. M. Prescott, J. M. Kim, G. A. Bliss, G. A. Zimmerman, and R. P. McEver. 1990. Nature (Lond). 343:757-760). We found that endothelial cells exposed to oxidants expressed GMP-140 on their surface, and that an mAb against GMP-140 or solubilized GMP-140 completely blocked PMN adherence to oxidant-treated endothelial cells. Thus, exposure of endothelial cells to oxygen radicals induces the prolonged expression of GMP-140 on the cell surface, which results in enhanced PMN adherence.
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PMID:Oxygen radicals induce human endothelial cells to express GMP-140 and bind neutrophils. 170 76

Phorbol esters which activate protein kinase C (PKC) have been shown to enhance experimental lung metastasis. Therefore, it was reasoned that inhibitors of PKC might also modulate metastasis. We have investigated this possibility using a PKC inhibitor, MDL 27,032 [4-propyl-5(4-pyridinyl)-2(3H)-oxazolone], as well as staurosporine and H-7. Treatment of B16F1 murine melanoma cells with MDL 27,032 for 24 h in culture and subsequent i.v. injection of the cells into mice resulted in greater than 90% inhibition of lung metastasis. Inhibition of metastasis was time dependent, with 90% of maximum inhibition occurring by 8 h of incubation. The 50% inhibitory concentration (IC50) for inhibition of metastasis with MDL 27,032 was 7 microM, a value similar to that for the inhibition of B16F1 membrane-associated PKC (IC50 = 13 microM) but not cytosolic PKC (IC50 = 54 microM). B16F1 cells treated with MDL 27,032 for 24 h were less adherent than untreated cells to extracellular matrix/basement membrane proteins. Adhesion to fibrinogen and collagen IV was inhibited (IC50 = 6 microM and 48 microM, respectively) by MDL 27,032, whereas adherence to laminin and fibronectin was not affected, indicating that the drug affects specific adhesion molecules. MDL 27,032-treated cells were also found to be less adherent than untreated cells to human umbilical vein endothelial cells. The phosphorylation of an 80-kDa B16F1 cell plasma membrane protein was stimulated under conditions known to stimulate PKC activity, and MDL 27,032 inhibited this phosphorylation in a dose-dependent manner. MDL 27,032 was more potent than H-7 for the inhibition of metastasis but was significantly less potent than staurosporine. These results support the hypothesis that there is a critical role for PKC-mediated phosphorylation of cell surface adhesion receptors in metastasis.
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PMID:Inhibition of experimental metastasis and cell adhesion of B16F1 melanoma cells by inhibitors of protein kinase C. 173 79

Fertilization in Chlamydomonas reinhardtii is initiated when gametes of opposite mating types adhere to each other via adhesion molecules (agglutinins) on their flagella. Adhesion leads to loss of active agglutinins from the flagella and recruitment of new agglutinins from a pool associated with the cell body. We have been interested in determining the precise cellular location of the pool and learning more about the relationship between agglutinins in the two domains. In the studies reported here we describe methods for purification of mt+ cell body agglutinins by use of ammonium sulfate precipitation, chromatography (molecular sieve, ion exchange, and hydrophobic interaction), and sucrose gradient centrifugation. About 90% of the total agglutinins were associated with the cell body and the remainder were on the flagella. Cell body agglutinins were indistinguishable from mt+ flagellar agglutinins by SDS-PAGE, elution properties on a hydrophobic interaction column, and in sedimentation properties on sucrose gradients. The nonadhesiveness of cell bodies suggested that the cell body agglutinins would be intracellular, but our results are not consistent with this interpretation. We have demonstrated that brief trypsin treatment of deflagellated gametes destroyed all of the cell body agglutinins and, in addition, we showed that the cell body agglutinins were accessible to surface iodination. These results indicated that C. reinhardtii agglutinins have a novel cellular disposition: active agglutinins, representing approximately 10% of the total cellular agglutinins, are found only on the flagella, whereas the remaining 90% of these molecules are on the external surface of the cell body plasma membrane in a nonfunctional form. This segregation of cell adhesion molecules into distinct membrane domains before gametic interactions has been demonstrated in sperm of multicellular organisms and may be a common mechanism for sequestering these critical molecules until gametes are activated for fusion. In experiments in which surface-iodinated cell bodies were permitted to regenerate new flagella, we found that the agglutinins (as well as the 350,000 Mr, major flagellar membrane protein) on the newly regenerated flagella were iodinated. These results indicate that proteins destined for the flagella can reside on the external surface of the cell body plasma membrane and are recruited onto newly forming flagella as well as onto preexisting flagella during fertilization.
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PMID:Cell body and flagellar agglutinins in Chlamydomonas reinhardtii: the cell body plasma membrane is a reservoir for agglutinins whose migration to the flagella is regulated by a functional barrier. 217 Apr 24

We have shown previously that Klebsiella pneumoniae receptors for coliphages T3 and T7 also mediate mannose-inhibitable adherence to human epithelial cells and protect bacteria from phagocytosis and intracellular killing by human polymorphonuclear cells. In this paper we analyze the possible role of such mannose-inhibitable adhesins and T3-T7 receptors (MIAT) in K. pneumoniae intraperitoneal pathogenicity for mice. We showed that intraperitoneal pathogenicity for mice of four different Klebsiella strains (one laboratory and three wild-type) that carry the MIAT was approximately 60-fold higher than that of four derivative strains that lost such receptors by spontaneous mutation. The MIAT could be repressed by Klebsiella phage AP3 lysogenic conversion. Two laboratory and two wild-type strains converted by phage AP3 were also approximately 60-fold less pathogenic for mice than parental strains and showed a pathogenicity level equal to that of the MIAT-negative mutants. Studies of protection in mice with anti-whole cell antisera showed that passive immunization against MIAT-positive cells was more protective than immunization against MIAT-negative cells. Studies of protection in mice by both active and passive immunization with lipopolysaccharide and purified outer membrane proteins have shown that the proteins are the most protective outer membrane components. Since it has been shown previously that the Klebsiella receptors for T3-T7 have a proteic component and that an outer membrane protein is missing in the strains resistant to T3-T7 (C. Pruzzo et al., in R. C. Berkely (ed.), Microbial Adhesion to Surfaces, 1980); the latter finding further supports the role of MIAT in the pathogenicity of Klebsiella for mice.
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PMID:Laboratory and wild-type Klebsiella pneumoniae strains carrying mannose-inhibitable adhesins and receptors for coliphages T3 and T7 are more pathogenic for mice than are strains without such receptors. 633 80

Platelet glycoprotein VI (GPVI), a 62kD membrane protein, has been identified as one of the platelet receptors for collagen, since GPVI-deficient platelets exhibit abnormal responses to collagen and an abnormal bleeding tendency. We report a female patient with a mild bleeding history whose platelets expressed 10% GPVI of normal platelets. Shape change, aggregation and ATP release of the patient's platelets were completely absent in response to 1-5 micrograms/ml collagen but present normally in response to ADP and Ca2+ ionophore A23187. Adhesion of the patient's platelets to coated collagen was mildly affected (40-60% of normal platelets) in spite of only 10% expression of GPVI. Flow cytometrical studies revealed that the patient's platelets expressed normal amounts of the GPIa/IIa complex. These results suggest that platelet GPVI is less involved in adhesion to collagen than shape change and aggregation induced by collagen.
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PMID:Platelets with 10% of the normal amount of glycoprotein VI have an impaired response to collagen that results in a mild bleeding tendency. 753 Apr 76

We investigated 49 acquired immunodeficiency syndrome-related lymphomas (ARLs) for Epstein-Barr virus (EBV) by Southern blotting and in situ hybridization and, in positive cases, used cryostat immunohistology to compare EBV-latent gene expression (EBV encoded small RNA-1 [EBER-1], EBV nuclear antigen-2 [EBNA-2], latent membrane protein-1 [LMP-1] and host cell immunophenotype (CD11a, CD18, CD54, CD58, CD21, CD23, CD30, CD39, CDw70, immunoglobulin) patterns with those reported in other EBV infections. EBV+ immunoblast-rich/large cell ARLs (n = 22) showed three patterns of latency: broad (EBER+EBNA-2+/LMP-1+; n = 9), reminiscent of a lymphoblastoid cell line phenotype; restricted (EBER+/EBNA-2-/LMP-1-; n = 6), similar to endemic Burkitt's lymphoma; and intermediate (EBER+/EBNA-2-/LMP-1+; n = 7), a pattern rarely described in vitro but seen in certain EBV-related malignancies. EBNA-2 expression was associated with extranodal lymphomas. EBV+ Burkitt-type ARLs (n = 11) usually showed the restricted latency pattern (n = 8), but some expressed the intermediate form (n = 3). Adhesion (CD54, CD58) and activation (CD30, CD39, CDw70) molecule expression varied with morphology (immunoblast-rich/large cell versus Burkitt-type), but was not independently correlated with EBV-positivity. CD30 and LMP-1 expression were associated. ARLs show heterogeneity regarding both the presence of EBV and latency pattern. Comparison of these phenotypically distinct lymphoma groups with known forms of EBV infection provides clues to their possible pathogenesis.
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PMID:Epstein-Barr virus-latent gene expression and tumor cell phenotype in acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma. Correlation of lymphoma phenotype with three distinct patterns of viral latency. 821 3

We report a non-HIV patient who had B chronic lymphocytic leukemia (CLL) with progressive multifocal leukoencephalopathy (PML) and diffuse cerebral leukemic parenchymal infiltration in the presence of JC virus and Epstein-Barr virus (EBV) cerebral co-infection. Multiple subcortical hypodensities lining the cortico-subcortical junction were present within the white matter on computerized tomography (CT) scan, with large areas of high signal intensity on T2-weighted sequences on magnetic resonance imaging (MRI). JCV DNA was identified in peripheral blood nuclear cells and cerebrospinal fluid polymerase chain reaction (PCR) DNA/DNA hybridization plus Southern blot analysis. Frontal stereotactic biopsy confirmed the diagnosis of PML by immunocytochemistry, in situ hybridization (ISH) with JC Enzo probe and electron microscopy. Leukemic B cells with the same phenotype as leukemic blood cells were disseminated in the demyelinated areas. They were labeled by anti-latent membrane protein and by BamHl W EBV probe after ISH. Adhesion and activation molecules were positive for CD23. Autopsy showed diffuse visceral leukemic infiltration without acutization. EBV-transformed B lymphocytes would favour JCV penetration and/or intracerebral reactivation of previously latent JCV infection with further development of simultaneous PML and cerebral CLL infiltration in an immunosuppressed patient.
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PMID:Simultaneous progressive multifocal leukoencephalopathy, Epstein-Barr virus (EBV) latent infection and cerebral parenchymal infiltration during chronic lymphocytic leukemia. 830 57

Adhesion molecules relate to cell invasion of autoimmune thyroid disease. We studied plasma soluble P-Selectin (platelet activation-dependent granule-external membrane protein), E-Selectin (endothelial leukocyte adhesion molecule) and L-Selectin (leukocyte endothelial cell adhesion molecule-1) levels in patients with Graves' disease before and during methimazole treatment. Plasma P-, E- and L-Selectin levels in patients with untreated Graves' disease were significantly higher than those in normal subjects. Plasma P-Selectin levels decreased when their thyroid functions were normal for more than 6 months after the start of methimazole treatment. No significant change in plasma E- and L-Selectin levels in patients with Graves' disease was found between hyperthyroid state and euthyroid state after the start of methimazole treatment, but plasma L-Selectin levels in patients with untreated Graves' disease were significantly lower than those in the patients in the first euthyroid state. There was no significant correlation between plasma P-Selectin levels and serum FT4 levels, nor between plasma P-Selectin levels and serum FT3 levels. These results suggested that thyroid hormones might reflect expression of P-, L- and E-Selectin from endothelial cells, or lymphocytes, or platelets in patients with Graves' disease.
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PMID:Plasma selectin levels in patients with Graves' disease. 907 11


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