Role of fibronectin in staphylococcal colonisation of fibrin thrombi and plastic surfaces

Abstract

Summary. The adhesive glycoprotein fibronectin has been proposed as a mediator of adherence of certain gram-positive cocci to host cells and fibrin thrombi. This study compared the role of soluble and immobilised fibronectin in the adherence of coagulasenegative staphylococci (CNS) and Staphylococcus aureus to fibrin thrombi and plastic surfaces. Adherence of S. epidermidis to fibrin thrombi was significantly reduced when fibronectin was removed from the plasma used for thrombus preparation. Adherence was restored through restitution of fibronectin. S. epidermidis also adhered substantially more to plastic surface coated with fibronectin than to non-coated plastic. Increased adherence of CNS to plastic was also observed after coating with the 29-kDa N-terminal fragment of fibronectin. Soluble fibronectin did not affect the adherence of CNS to fibrin thrombi or plastic surfaces. The adherence of S. aureus to fibrin thrombi was significantly increased by the addition of soluble fibronectin, but not by incorporation of fibronectin into the clot. These results indicate that the binding of fibronectin is an important factor in the adherence of staphylococci to fibrin clots and plastic surfaces and, thus, colonisation of these surfaces. However, the two species of staphylococci seem to employ different mechanisms of fibronectin-mediated adherence : S. epidermidis interacts mainly with fibronectin incorporated in fibrin clots or immobilised on implanted synthetic materials, whereas S. aureus adheres to the fibrin matrix through binding of soluble fibronectin present in wound exudates.

Different Effects of Fibronectin on the Phagocytosis of Staphylococcus aureus and Coagulase‐Negative Staphylococci by Murine Peritoneal Macrophages

“…Further, it is probable that these three strains have the same FN binding components, FnBPs. Both S. aureus and CNS strains are known to recognize the same 29-kDa N-terminal fragment of FN (30). This fragment binds to the Dregion of S. aureus FnBP.…”

Adhesion ofStaphylococcus epidermidis and transposon mutant strains to hydrophobic polyethylene

“…5,6 Other studies suggest that nonspecific interactions associated with biomaterial surface properties such as hydrophobicity and topography, or specific ligand-receptor interactions involving individual plasma proteins, platelets, and bacterial adhesins, are potentially important determining factors. [7][8][9][10][11][12] A capsular polysaccharide adhesin (PS/A) was isolated by Tojo et al, who demonstrated that strains of S. epidermidis expressing PS/A and slime adhered in greater numbers to Silastic catheter tubing than strains which did not express PS/A. 13 The subsequent generation of isogenic (PS/A−, slime−) transposon (Tn) mutant strains of the (PS/A+, slime+) parent strain S. epidermidis M187 allowed further examination of the role of PS/A and slime in S. epidermidis adhesion to polymer biomaterials.…”

Expression of slime interferes with in vitro detection of host protein receptors of Staphylococcus epidermidis

“…Some investigations have indicated that matrix proteins absorbed on the implant surface can support the adhesion of S. epidermidis strains to various polymers (14,19,23), while others could not detect any increment in the rates of CoagNS adhesion to either silicone tubing (17) or Teflon catheters (18). Conflicting data also exist regarding the possible contribution of surface hydrophobicity to the ability of CoagNS to infect biomaterial implants (1,11,15,22).…”