Specific binding of Staphylococcus aureus to cultured porcine cardiac valvular endothelial cells.
Infective endocarditis usually occurs in patients who have had previous cardiac damage or who have congenitally abnormal hearts. However, this infection may afflict otherwise normal individuals, and it is often caused by Staphylococcus aureus. In these individuals, interactions between circulating microorganisms and resident cardiac endothelial cells may initiate the infection. In the present studies we established an assay to measure in vitro binding of S. aureus to porcine cardiac valve endothelial cells. We found that this interaction was specific and saturable with respect to time. In contrast, there was no specific binding of Escherichia coli, an organism that rarely causes endocarditis. Exogenous fibronectin had no effect on specific binding of S. aureus, and heat-killed organisms adhered equally well as viable bacteria. Fixation of the endothelial cells with formalin abolished all specific binding. Soluble components from bacterial extracts inhibited S. aureus binding in dose-dependent fashion. These observations suggest that circulating S. aureus may interact with specific sites on cardiac endothelial cells, thereby potentially initiating infective endocarditis.
Johnson
C M
CM
Department of Pediatrics, Mayo Clinic and Foundation, Rochester, MN 55905.
Hancock
G A
GA
Goulin
G D
GD
D000818:Animals; D001422:Bacterial Adhesion; D002478:Cells, Cultured; D002701:Chloramphenicol / Q000494:pharmacology; D004697:Endocarditis, Bacterial / Q000382:microbiology; D004727:Endothelium / Q000166:cytology; D004926:Escherichia coli / Q000187:drug effects / Q000502:physiology; D005353:Fibronectins / Q000494:pharmacology; D006351:Heart Valves / Q000166:cytology*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000502:physiology*; D013552:Swine; D013997:Time Factors
D005353:Fibronectins; D002701:Chloramphenicol