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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

Activation of human umbilical vein endothelial (HUVE) cells with the inflammatory mediators tumour necrosis factor-alpha (TNF), interleukin-1 (IL-1), lipopolysaccharide (LPS) and phorbol esters enhanced their adhesiveness for leucocytes. The appearance of an activation antigen ELAM-1, recognized by a monoclonal antibody (MoAb) ENA1, parallels the kinetics of the enhanced adherence of leucocytes to endothelial cells. Adhesion of polymorphonuclear cells (PMN) to activated HUVE cells could be blocked by F(ab')2 fragments of MoAb ENA1 up to 60%. An additive inhibition of the adhesion was established by pre-incubation of the PMN with anti-CD18 MoAb and/or leucocyte adhesion inhibitor (LAI), produced by endothelial cells. An opposite reaction, however, was observed when HUVE cells were pre-incubated with intact MoAb ENA1, resulting in an enhancement of the adhesion up to 200%. Apparently, the blocking effect of MoAb ENA1 could be bypassed by the strong interaction of the Fc part of the MoAb with the Fc receptor (FcR) on the PMN. Similarly, anti-CD18 MoAb and/or LAI reduced the adhesion observed if intact ENA1 were used, and Fc-FcR interaction took place. The results presented in this study indicate that adhesion via ELAM-1, the CD18 antigen and via the receptor for LAI are different mechanisms. These mechanisms may act in concert to strengthen the binding of PMN to HUVE cells. Moreover, a strong adhesion could be established via the Fc part of MoAbs directed against HUVE cells with the FcR on the PMN. The phenomenon described may play a role in graft rejection and in diseases where antibodies directed against endothelium are involved.
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PMID:Adhesion of polymorphonuclear cells to human endothelial cells. Adhesion-molecule-dependent, and Fc receptor-mediated adhesion-molecule-independent mechanisms. 169

Interleukin 1 (IL-1), bacterial lipopolysaccharide (LPS) and tumor necrosis factor (TNF alpha) enhance the adherence properties of endothelial cells (EC) for neutrophils (PMN). This is mediated in part by the up-regulation of Intercellular Adhesion Molecule 1 (ICAM-1) on EC. Phorbol esters, which activate protein kinase c (PKC) and enhance the adherence properties of EC for PMN also up-regulate the ICAM-1 expression on EC. We investigated the effect of PKC inhibitors on ICAM-1 expression of human umbilical vein EC (HUVEC). Staurosporine (STS) and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) prevented inflammatory mediator-dependent stimulation of both ICAM-1 expression and PMN adherence by HUVEC (ID50 for STS = 2.7-2.9 microM; for H-7 = 7.6-8.8 microM). Inhibition was dose and time-dependent and was not due to HUVEC toxicity. The STS analog K252a and the H-7 analog W-7 were less potent inhibitors of ICAM-1 up-regulation and adherence promotion. Prolonged exposure of HUVEC to phorbol myristate acetate down-regulated PKC activity and inhibited subsequent ICAM-1 up-regulation by this agent and by IL-1. We conclude that inflammatory mediator induced stimulation of HUVEC expression of ICAM-1 and promotion of adherence properties are mediated in part by activation of PKC.
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PMID:Protein kinase C inhibitors block the enhanced expression of intercellular adhesion molecule-1 on endothelial cells activated by interleukin-1, lipopolysaccharide and tumor necrosis factor. 224 11

Adhesion of Campylobacter jejuni and C. coli to epithelial cells is thought to be a decisive step in enteritis. In this work, we tried to determine which bacterial components are responsible for this phenomenon. Outer membrane (OM) extracts were prepared from strains of C. jejuni (3 strains) and C. coli (2 strains). These strains had been isolated from stools of febrile patients with diarrhoea and were able to adhere to HeLa cells in culture. After incubation of bacterial OM extracts with HeLa cells in culture, bacterial adherent material was recovered, subjected to electrophoresis and immunoblotted. Bacterial adherent antigens were revealed by a rabbit antiserum raised against whole bacterial cells. Antigenic fractions, ranging from 26 to 30 kDa, were found to preferentially bind to HeLa cells (cell-binding fractions; CBF). These antigens were proteins and were distinct from flagellin and lipopolysaccharide. Bacteria incubated with a rabbit antiserum raised against homologous CBF, were unable to bind to HeLa cells. Moreover, the inhibitory effect decreased when the antiserum was diluted. Under the same conditions, a rabbit antiserum raised against a non-adherent OM fraction of 92 kDa did not prevent bacteria from binding to HeLa cells.
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PMID:Adhesion to HeLa cells of Campylobacter jejuni and C. coli outer membrane components. 261 91

We here report that interleukin 4 (IL-4) alone is able to induce cellular adhesion among mouse lymphocytes, and together with lipopolysaccharide (LPS), it increases the adhesion induced by LPS. The adhesion was inhibited by antibodies against IL-4. IL-4 appears to be acting mainly on B lymphocytes, since the response caused by IL-4 alone was much less sensitive to depletion of adherent cells than the LPS response. Depletion of T cells had no effect on IL-4- or LPS-induced adhesion. IL-4 could together with Con A, but not alone, induce adhesion among T cells. Cell clusters, which were formed after 2-3 days of LPS plus IL-4 stimulation, could be completely dissociated, and when the cells were recultured in medium, they readily started to reaggregate. The adhesion molecule lymphocyte function-associated antigen 1 (LFA-1) is, at least in part, involved in LPS plus IL-4-induced adhesion. Antibodies against LFA-1 inhibited the adhesion, but antibodies against other cell surface molecules were without inhibitory effect. Adhesion induced by IL-4 alone may involve other adhesion molecules than LFA-1.
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PMID:Interleukin 4 induces cellular adhesion among B lymphocytes. 269 70

Adhesion to and penetration of HeLa cell monolayers by Salmonella typhi Ty2 requires the presence of a complete lipopolysaccharide as demonstrated by the inability of polysaccharide-defective mutants to invade the monolayer. Lysis of HeLa cell monolayers by Salmonella typhi Ty2 is associated with intracellular bacterial multiplication and no detectable production of extracellular toxins. The ability of Salmonella typhi to invade and lyse monolayers could provide a novel system for the study of its ability to invade the bloodstream from the intestine.
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PMID:Invasion and lysis of HeLa cell monolayers by Salmonella typhi: the role of lipopolysaccharide. 271 13

Intercellular adhesion molecule-1 (ICAM-1) on the surface of cultured umbilical vein and saphenous vein endothelial cells was upregulated between 2.5- and 40-fold by rIL-1, rTNF, LPS and rIFN gamma corresponding to up to 5 X 10(6) sites/cell. Endothelial cell ICAM-1 was a single band of 90 kD in SDS-PAGE. Purified endothelial cell ICAM-1 reconstituted into liposomes and bound to plastic was an excellent substrate for both JY B lymphoblastoid cell and T lymphoblast adhesion. Adhesion to endothelial cell ICAM-1 in planar membranes was blocked completely by monoclonal antibodies to lymphocyte function associated antigen-1 (LFA-1) or ICAM-1. Adhesion to artificial membranes was most sensitive to ICAM-1 density within the physiological range found on resting and stimulated endothelial cells. Adhesion of JY B lymphoblastoid cells, normal and genetically LFA-1 deficient T lymphoblasts and resting peripheral blood lymphocytes to endothelial cell monolayers was also assayed. In summary, LFA-1 dependent (60-90% of total adhesion) and LFA-1-independent basal adhesion was observed and the use of both adhesion pathways by different interacting cell pairs was increased by monokine or lipopolysaccharide stimulation of endothelial cells. The LFA-1-dependent adhesion could be further subdivided into an LFA-1/ICAM-1-dependent component which was increased by cytokines and a basal LFA-1-dependent, ICAM-1-independent component which did not appear to be affected by cytokines. We conclude that ICAM-1 is a regulated ligand for lymphocyte-endothelial cell adhesion, but at least two other major adhesion pathways exist.
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PMID:Lymphocyte function-associated antigen-1 (LFA-1) interaction with intercellular adhesion molecule-1 (ICAM-1) is one of at least three mechanisms for lymphocyte adhesion to cultured endothelial cells. 313 64

Escherichia coli F-18 isolated from the feces of a healthy human is an excellent colonizer of the CD-1 mouse colon. In the present investigation, adhesion of E. coli F-18 to CD-1 mouse colonic mucus and bovine serum albumin (BSA), immobilized on polystyrene, was studied. Adhesion of E. coli F-18 to mucus was two- to sixfold greater than to either BSA or polystyrene. E. coli F-18 lipopolysaccharide specifically blocked adhesion of E. coli F-18 to mucus and mimicked adhesion of E. coli F-18 to mucus, BSA, and polystyrene. Purified capsule also blocked adhesion of E. coli F-18 to mucus, but this inhibition was found to be entirely nonspecific. The specific E. coli F-18 receptor in mucus appeared to be a glycoprotein, containing sugars normally found in mucins and having a maximum molecular weight of between 1.25 X 10(5) and 2.5 X 10(5).
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PMID:Adhesion of a human fecal Escherichia coli strain to mouse colonic mucus. 392 Jan 46

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

A comparative study of leukocyte adhesion to the endothelium of the thoracic aorta and left carotid artery in rats has been performed after administration of two hyperlipidemic diets for 15 days, proinflammatory agents (thrombin, lipopolysaccharide and zymosan activated serum) and plasma expanders [dextran, polyvinylpyrrolidone (PVP), rat albumin and several bovine albumins from different sources]. Leukocytes adhered to the endothelium were demonstrated in surface preparations by esterase activity. Activation of circulating leukocytes was measured by nitroblue tetrazolium reduction and luminol enhanced chemiluminescence. Both hyperlipidemic diets produced, in all rats, more leukocyte adhesion in the aorta than in the carotid artery. All proinflammatory agents produced at 1 h, increases in leukocyte adhesion--which in all rats were greater in the carotid artery than in the aorta--and leukocyte activation, which was higher at 3 h than at 1 h. Dextran, PVP, bovine albumins 103700 and A-4503 at 18 h produced slight increases in leukocyte adhesion in the aorta but not in the carotid artery. Rat albumin and bovine albumin A-7906 determined an intense leukocyte adhesion at 18 h which was not preferential to either vessel. Adhesion produced by A-7906 was maximal at 12 h and partially inhibited by dexamethasone. This last albumin produced leukocyte activation at 3 h and was sequestered 5 min after administration, reaching normal values at 1 h. Albumins 103700 and A-4503 neither activated leukocytes nor were sequestered after administration.
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PMID:Effect of hyperlipidemic diets, proinflammatory agents and plasma expanders on leukocyte adhesion to the endothelium of aorta and carotid artery of rats. 753 42


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