Adsorption of fibronection to Teflon followed byS. aureus adherence

Abstract

Group B streptococcus can be a serious infection of neonates and, in the past, specific antibody has been shown to mediate immunity against this organism. However, specific antibody is not required for phagocytosis of highly pathogenic organisms by neutrophils. Furthermore, the bacteria subsequently survive and tend to accumulate or multiply in these cells, which they then disrupt. Highly pathogenic streptococci are killed by neutrophils in the presence of specific antibody. Moreover, the addition of specific antibody to neutrophils after phagocytosis of the organisms had occurred stimulated the phagocytes to kill the ingested bacteria. This post-phagocytic role for antibody in the killing of bacteria by neutrophils, as opposed to their ingestion, has not been previously described. Once inside the cell, specific antibody binds to protective surface determinants on the bacteria and allows the organisms to be killed. Present work involves an examination of the surface virulence determinants that are responsible for the survival of highly pathogenic group B streptococci within neutrophils. Adsorption of fibronectin to Teflon followed by S.aureus adherenceInfection of implanted prostheses or catheters represent a major problem in modern medicine. We have recently demonstrated that fibronectin (FN) is an important ligand of Staphylococcus aureus adherence to polymethylmethacrylate (PMMA) material, which was implanted into animals and used as an experimental model of foreign body infection (J. infect. Dis. 150, 546). In a related in vitro study, we described FN adsorption by PMMA coverslips (J. infect. Dis. 45, 768). Using similar techniques, we studied quantitative adsorption of 125I-labeled FN and promotion of S. aureus adherence onto Teflon | which is a widely used material in the clinic. The adsorption of purified FN for Teflon was dose-dependent and resembled that for PMMA. Promotion of S. aureus adherence by Teflon | adsorbed FN was dose-dependent, leading to increased bacterial adherence up to a maximum of 6.5 x 104 bacteria per coverslip. In contrast, Teflon unexposed to FN bound 3 • 103 bacteria by coverslip. FN adsorption on Teflon | and its promotion of bacterial adherence were prevented by other serum proteins ( = FN-depleted serum pool). In summary, FN adsorption and its promotion of S. aureus adherence by Teflon are similar to those found previously with PMMA.A prospective study of urinary tract infections in long-term catheterized spinal injury patients revealed their complexity. Mixed bacterial communities of up to eight multi-drug resistant species were commonly isolated. In the absence of chemotherapy some species were persistent and others transient inhabitants. In vitro, tests showed that there was no correlation between adherence of the bacteria to bladder uroepithelial cells and persistence. Pseudomonas aeruginosa gave significantly higher adherence to silicone-and teflon-coated catheter sections than all the other isolates. Overall however there was no relationship between persistence and the abi...

Role of Host and Bacterial Factors in Modulating Staphylococcal Adhesion to Implanted Polymer Surfaces

“…In contrast to these data, we [4,[8][9][10][11][12][13] and others [1,14,15] have found that plasma proteins strongly interfered with bacterial adhesion to polymer surfaces: indeed, the presence of either whole plasma [14] or serum [8,15], or of purified albumin [8][9][10][11][12][13] in the adhesion medium prevented staphylococcal adhesion to the native polymer surfaces. This serum protein-mediated inhibition of bacterial adhesion was observed with a range of different materials, such as PMMA [8,9,12,13], Teflon [10], fluorinated polyethylene-propylene films [14] and polyvinylchloride (PVC [11]) and with a number of clinical [12,14] and laboratory isolates [8][9][10][11]13] of staphylococci. Except for one study performed with tissue culture plates [111, we used for the others [8][9][10]12,13] a single type of in vitro experimental assay, which tested various staphylococcal strains for adhesion to small-sized polymer surfaces: coverslips (1 x 1 cm) made of either PUMA or ~flon were incubated in a shaking waterbath of 60 min at 37°C with calibrated suspensions of staphylococci containing generally 4 x 106 organisms/ml [8][9]…”

“…It is difficult to speculate from these in vitro data on the possible role in vivo of either surface-bound collagen or laminin as promoting directly staphylococcal adhesion. At least, we can say that collagen has an important role to play on staphylococcal adhesion as a cofactor, because it can promote adsorption of fibronectin on the surface of biomaterials [4,9,10]. Furthermore, fibronectin adsorbed on denatured collagen or gelatin layers shows an improved biological activity over fibronectin adsorbed on native polymers [4,9,10].…”

“…Except for one study performed with tissue culture plates [111, we used for the others [8][9][10]12,13] a single type of in vitro experimental assay, which tested various staphylococcal strains for adhesion to small-sized polymer surfaces: coverslips (1 x 1 cm) made of either PUMA or ~flon were incubated in a shaking waterbath of 60 min at 37°C with calibrated suspensions of staphylococci containing generally 4 x 106 organisms/ml [8][9][10]12,13]. After rinsing of the unbound organisms using 'previously described procedures [8][9][10]12,13], we estimated the number of surface-adherent organisms by radioactive counts of the (3 H)thymidine-labeled staphylococcal culture.…”

“…Since surface-bound fibronectin appeared as an important factor promoting adhesion of staphylococci via specific binding sites located on the bacterial surface [17], we further studied this interaction by using a simplified in vitro assay [9]: unimplanted PMMA [9] or Teflon [10] coverslips were incubated with purified fibronectin in solution, resulting in a permanent surface coating by this protein. The extent of fibronectin bound to the polymer surface was estimated by radioactive counts of the 125I-Iabeled protein [9], yielding a saturable, dose-dependent response [9,10].…”

“…The extent of fibronectin bound to the polymer surface was estimated by radioactive counts of the 125I-Iabeled protein [9], yielding a saturable, dose-dependent response [9,10]. Promotion of S. aureus [9,10] or S. epidermidis [13] adhesion by surface-bound fibronectin was also dose-dependent. Adhesion assays were all performed in the presence of 5 mg/ml human albumin, which prevented bacterial deposition on polymers uncoated with fibronectin, but showed no effect on fibronectin-mediated adhesion [9-13J.…”