Monosaccharide Inhibition of Staphylococcus aureus Adherence to Human Solid-Phase Fibronectin

Host Factors Selectively Increase Staphylococcal Adherence on Inserted Catheters: A Role for Fibronectin and Fibrinogen or Fibrin

“…These data extend our previous results showing a general inhibition by albumin of staphylococcal adherence to native polymers, which applies to all types of materials and species of staphylococci tested thus far [48][49][50][51][52]. Work in progress in our laboratory indicates also that the recently introduced polyurethane cannulae do not allow significant adherence of the three laboratory strains of staphylococci and of the 10 bacteremic isolates from iv device infections.…”

“…The various catheter materials tested -the short Teflon and long PVC peripheral lines -reacted much as did PMMA [48,49] and Teflon [50] coverslips and PVC tissue culture plates [51]. For all native, uninserted materials tested, whatever their shape, the presence of albumin in the incubation medium or on the surfaces of the material prevented staphylococcal adherence.…”

“…More recent studies have extended these observations to other types of biomaterials [50,51], protein coats [52], and staphylococcal strains tested: most clinical isolates associated with intravenous device infections showed increased adherence in this experimental system [52]. In particular, 0 of 27 coagulase-positive and -negative bacteremic isolates from intravenous device infections could attach to the native polymers coated with whole serum or albumin [52] whereas adherence of all clinical isolates was restored by coating the polymers with fibronectin [52].…”

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]…”

“…137 Fibronectin-mediated adhesion of the protein A-negative strains S. aureus Wood 46 and S. epidermidis KH 11 was also [4,8,24] sensitive to inhibition by anti-fibronectin antibodies (Figure 1), as observed with implanted coverslips. This antibody-mediated inhibition appears to be specific for anti-fibronectin antibodies, since anti-fibrinogen immunoglobulins do not modify adhesion of either S. aureus Wood 46 or S. epidermidis KH 11 (Figure 1). …”