Bacterial adherence to fibronectin and endothelial cells: a possible mechanism for bacterial tissue tropism

Gregory M. Vercellotti, Daniel Lussenhop, Phillip K. Peterson, Leo T. Furcht, James B. McCarthy, Harry S. Jacob, Charles F. Moldow

Research output: Contribution to journalArticlepeer-review

89 Scopus citations

Abstract

In the pathophysiology of endocarditis, bacteria must initially adhere to the endothelial surface components of the cardiac valve before invasion and colonization. The attachment of bacteria to endothelial cell surfaces is dependent on surface characteristics of both the bacteria and the endothelial cell. Fibronectin, a glycoprotein produced by endothelial cells, binds to some bacteria but not all. This report examines bacterial adherence to human endothelial cells and to fibronectin-coated surfaces. Radiolabeled Staphylococcus aureus (Cowan I strain) and viridans streptococci avidly bound to fibronectin-coated surfaces and endothelial cell monolayers. In contrast, gram-negative organisms such as Escherichia coli bound poorly to both substrates. The adherence of S. aureus was dependent on time as well as on the concentration of fibronectin or the endothelial cell number. Bacterial adherence was specific for endothelial cells or fibronectin, since none occurred to plastic or to wells coated with collagen or albumin. The binding of S. aureus to fibronectin or endothelial cells appeared dependent on a bacterial surface protein, since treatment of the bacteria with proteases markedly decreased adherence. S. aureus was not dependent on the protein A or teichoic acid content of the cell wall, but adherence was markedly decreased in bacterial strains that had a carbohydrate capsule. S. aureus pretreated with serum or purified fibronectin manifested enhanced adherence to endothelial cells, suggesting fibronectin-fibronectin interactions. Bacteria specifically attach to endothelial cells and to fibronectin-coated surfaces, which suggests that the ability of a bacterium to attach to these substrates may reflect the propensity to invade and colonize vascular tissues such as cardiac valves.

Original languageEnglish (US)
Pages (from-to)34-43
Number of pages10
JournalThe Journal of laboratory and clinical medicine
Volume103
Issue number1
StatePublished - Jan 1984

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