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

A study was undertaken to investigate the factors involved in the adhesion of Pseudomonas fluorescens to model meat surfaces (tendon slices). Adhesion was fast (less than 2.5 min) and was not suppressed by killing the cells with UV, gamma rays, or heat, indicating that physiological activity was not required. In various salt solutions (NaCl, KCl, CaCl2, MgCl2), adhesion increased with increasing ionic strength up to 10 to 100 mM, suggesting that, at low ionic strengths, electrostatic interactions were involved in the adhesion process. At higher ionic strengths (greater than 10 to 100 mM) or in the presence of Al3+ ions, adhesion was sharply reduced. Selectively blocking of carboxyl or amino groups at the cell surface by chemical means did not affect adhesion. These groups are therefore not directly involved in an adhesive bond with tendon. Given a sufficient cell concentration (10(10) CFU.ml-1) in the adhesion medium, the surface of tendon was almost entirely covered with adherent bacteria. This suggests that if the adhesion is specific, the attachment sites on the tendon surface must be located within collagen or proteoglycan molecules.
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PMID:A model study of factors involved in adhesion of Pseudomonas fluorescens to meat. 144 87

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

Activated polymorphonuclear leukocytes (PMNs) are implicated in the pathogenesis of acute lung injury (ALI) associated with sepsis. Adhesion of activated PMNs to endothelial monolayers is mediated by the CD18 adhesion-receptor complex on the PMN cell surface. Monoclonal antibody 60.3 (MoAb 60.3) blocks CD18-dependent PMN-endothelial adhesion in vitro and in vivo. This study was designed to determine the role of CD18-dependent PMN adhesion in ALI associated with gram-negative sepsis. Anesthetized, ventilated (FiO2 0.5, positive end-expiratory pressure 5 cm H2O) pigs received sterile saline (control, n = 8) or live Pseudomonas aeruginosa, 5 x 10(8) colony-forming units/ml at 0.3 ml/20 kg/min (septic, n = 9) for 1 hour. A third group (n = 7) received MoAb 60.3, 2 mg/kg intravenously, 15 minutes before Pseudomonas infusion. Animals were studied for 300 minutes. MoAb 60.3 significantly (p less than 0.05) attenuated the neutropenia seen in sepsis (15 +/- 1 vs 6 +/- 1 x 10(3) PMNs/mm3 at 300 min). Alveolar-capillary membrane injury was assessed by bronchoalveolar-lavage protein content and extravascular lung water determination. MoAb 60.3 significantly (p less than 0.05) reduced BAL protein at 300 minutes (388 +/- 75 vs 1059 +/- 216 micrograms/ml in septic animals) and attenuated the increase in extravascular lung water to 240 minutes (7.1 +/- 2 vs 14.2 +/- 1.2 ml/kg in septic animals). Systemic hypotension, decreased cardiac index, pulmonary hypertension, and relative hypoxemia, all characteristic of this model, were not altered by MoAb 60.3. These data suggest that, in this model of septic ALI, neutropenia is, in part, CD18 dependent and that blocking CD18-dependent PMN adhesion protects the alveolar-capillary membrane independently of altered hemodynamic status.
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PMID:Anti-CD18 antibody attenuates neutropenia and alveolar capillary-membrane injury during gram-negative sepsis. 167 91

The composition of the bacterial flora in the upper respiratory tract is closely correlated with the type of pathogens recovered from the respiratory tract in patients. In intensive care patients, colonization of the oral cavity with Gram-negative organisms increases the risk of Gram-negative respiratory tract infection; the ability of bacterial cells to attach to buccal cells seems to play a central role in this correlation. Similar findings have been reported in chronic respiratory tract infections, including bronchiectasis and cystic fibrosis, with Pseudomonas aeruginosa colonization. This study was undertaken to determine the conditions best suited to in vitro detection of adhesion of P. aeruginosa to buccal cells. Use of brain-heart-infusion medium, incubation at 35 degrees C for 2 hours, and a bacterial concentration of 2 x 10(9) cells/ml were the factors correlated with improved detection of adhesion to buccal cells. Furthermore, attachment of bacteria to buccal cells was not found to vary across donors or over time in a given donor. Adhesion was independent of cell viability.
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PMID:[Determination of factors promoting, in vitro, the expression of adhesion of Pseudomonas aeruginosa to buccal cells]. 190 7

The present study was designed to examine the effect of Pseudomonas aeruginosa alkaline protease (AP) and elastase (Ela) on human natural killer (NK) cell activity in vitro. AP and Ela were found to inhibit NK cell function. Addition of alpha interferon and interleukin-2 did not abolish this inhibition of NK cell activity. Adhesion of effector to target cells was studied in a single-cell agarose assay of monocyte-depleted NK-cell-enriched cell populations. AP and Ela were shown to inhibit effector/target cell conjugate formation. Furthermore, AP and Ela inhibited the binding of the monoclonal antibody Leu-11, which reacts with the Fc receptor of NK cells. The inhibition of NK cell binding to the target cell by P. aeruginosa proteases is most likely due to proteolytic cleavage of the surface receptors involved in the binding of the effector cell to the target cell.
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PMID:Inhibition of human natural killer cell activity by Pseudomonas aeruginosa alkaline protease and elastase. 303 Sep 37

Comparison was made of the adhesion of Staphylococcus epidermidis, Staphylococcus aureus, Escherichia coli, Klebsiella aerogenes and Pseudomonas aeruginosa to six types of intravascular cannula material. Adhesion to materials removed from rabbit tissues did not differ significantly between types of material or between bacterial species. In contrast, major differences were found when unimplanted materials were examined; the overall rank order of adhesiveness of bacteria to unimplanted materials (S. epidermidis greater than P. aeruginosa greater than S. aureus much greater than K. aerogenes greater than E. coli) was highly significant (F = 13.0, P less than 0.0005), and although no single material was consistently least attractive to all micro-organisms, FEP-Teflon and PTFE-Teflon showed significantly lower overall affinity for bacteria than other materials (P less than 0.001); all species showed a significant preference for a silicone polymer (P less than 0.0005). The nature of the bacterial surface structures responsible for adhesion were investigated by the actions of pronase and mixed glycosidase, which produced significant respective decreases and increases in adhesion of staphylococci to unimplanted materials; their effects on the Gram-negative bacilli were less consistent.
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PMID:Bacterial adhesion to intravenous cannulae: influence of implantation in the rabbit and of enzyme treatments. 312 62

The relationship between the variability in the fibronectin (Fn) content on human buccal epithelial cells and the capacity of the cells to bind gram-positive (Streptococcus pyogenes) or gram-negative (Escherichia coli or Pseudomonas aeruginosa) bacteria was investigated. Adhesion experiments performed with mixtures of epithelial cells and mixed suspensions of either S. pyogenes and E. coli or S. pyogenes and P. aeruginosa exhibited three major populations of buccal cells: one of these was able to bind S. pyogenes (gram positive) but neither of the gram-negative bacteria; a second population was able to bind the gram-negative but not the gram-positive bacteria; and a third was able to bind various numbers of both types of organisms. Further adhesion experiments performed with a mixture of epithelial cells and a mixed suspension of S. pyrogens, E. coli, and fluoresceinconjugated methacrylate beads coated with immune immunoglobulin G directed against Fn revealed that the epithelial cells recognizing the gram-positive bacteria were rich in Fn, whereas those recognizing the gram-negative organisms were poor in Fn. Immunoelectron microscopy confirmed that cells of S. pyogenes bound to epithelial cells coated with Fn, whereas cells of E. coli bound to epithelial cells lacking Fn. These results suggest that Fn on the surfaces of epithelial cells may modulate the ecology of the human oropharyngeal cavity, especially with respect to the colonization of these surfaces by pathogenic gram-negative or gram-positive bacteria.
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PMID:Adherence of streptococcus pyogenes, Escherichia coli, and Pseudomonas aeruginosa to fibronectin-coated and uncoated epithelial cells. 641 21

FIZ15 phage of Pseudomonas aeruginosa causes lysogenic conversion in PAO1 strain. Lysogen shows increased adhesion to human buccal epithelial cells, increased resistance to 75 percent human serum bactericidal effect, and streptomycin resistant. These phenotypes apparently are due to a phage-induced superficial change on its own bacterial receptor, which probably is the O-antigen. In order to begin FIZ15 characterization, nitrous acid-induced clear-plaque mutants were obtained. They belonged to three complementation groups and mapping by two factor crosses revealed that they were closely linked. In a search for phage mutants that do not cause lysogenic conversion, two streptomycin-sensitive mutants were obtained by ethyl methane sulphonate mutagenesis of PAO1 lysogenic for FIZ15 (PIZ15 strain). One mutant (con1) showed and adhesion value similar to that of PAO1 and the other (con2) had an adhesion twofold and 1.3 times greater than PAO1 and PIZ15, respectively. con1 did not show increased serum resistance, whereas con2 was as resistant as PIZ15. Phages were isolated from the streptomycin sensitive mutants and used to relisogenize PAO1 to obtain the con1d and con2d lysogens. Adhesion and serum sensitivity of con1d was identical to that of PAO1 but con2d behaves like PIZ15. FIZ15 phage was unable to adsorb to PIZ15, con2 and con2d. On the other hand, FIZ15 phage adsorbs well to con1 and con1d but not to PIZ15. These results suggest that con1 mutation lies on the phage chromosome and con2 on the bacterial one. Finally, adhesion of all lysogens and PAO1 was stimulated 2-3 times by KCl and this effect was suppressed by and oxidative phosphorylation uncoupler.
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PMID:Partial genetic characterization of FIZ15 bacteriophage of Pseudomonas aeruginosa. 804 27

Adherence of Pseudomonas aeruginosa to cells of the respiratory tract of patients with cystic fibrosis (CF) appears to be a necessary precondition for colonization and infection. To date no effective anti-adhesive strategy has been devised for preventing P. aeruginosa infection in these vulnerable hosts. The purpose of these studies was to evaluate the potential for preventing adhesion of P. aeruginosa to epithelial cells with dextran. Dextran (3,000-70,000 MW) inhibited adhesion of P. aeruginosa to buccal and A549 pulmonary epithelial cells; the 3,000 MW compound, at 10 mM was most inhibitory. Adhesion was inhibited optimally at pH 7.4 and was independent of charge; dextran and dextran sulfate were equally inhibitory. Dextran was most inhibitory if added to the epithelial cells before the P. aeruginosa; adhesion was reversed only minimally by adding dextran after the bacteria were bound. The inhibitory effect appeared to be nonspecific because other neutral polysaccharides (glycogen and mannan) were also inhibitory, dextran blocked attachment of other respiratory tract pathogens (Staphylococcus aureus, Group A streptococcus, and Haemophilus influenzae), and because dextran did not bind specifically to bacteria or to epithelial cells. Dextran is an inexpensive and nontoxic agent and may be useful in patients with CF to prevent colonization and infection with P. aeruginosa.
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PMID:Inhibition by dextran of Pseudomonas aeruginosa adherence to epithelial cells. 897 Mar 72

Adhesion of bacteria to hydrogel lenses is thought to be an initial step of ocular colonization allowing evasion of normal host defences. The salt concentration of media is an important parameter controlling microbial adhesion. Salinity varies from 0.97% NaCl equivalents in the open eye to 0.89% in the closed eye state. In this study, the effect of sodium chloride in the concentration range of 0.8-1.0% (w/v) NaCl on adhesion of ocular bacteria to soft contact lenses was investigated using a static adhesion assay. Pseudomonas aeruginosa was found to adhere to lenses in significantly greater amounts than Serratia marcescens, Flavobacterium meningosepticum, Stenotrophomonas maltophilia and Staphylococcus intermedius. Increasing NaCl from 0.8% to 1.0% (w/v) increased adhesion of all bacteria tested. This adhesion was strong since the organisms could not be removed by washing in low ionic buffer. Adhesion of these organisms did not correlate with their cell surface properties as determined by bacterial adhesion to hydrocarbons (BATH) and retention on sepharose columns.
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PMID:A relatively small change in sodium chloride concentration has a strong effect on adhesion of ocular bacteria to contact lenses. 971 79


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