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Abstract
Staphylococcus aureus secretes products that convert host fibrinogen to fibrin and promote its agglutination with fibrin fibrils, thereby shielding bacteria from immune defenses. The agglutination reaction involves ClfA (clumping factor A), a surface protein with serine-aspartate (SD) repeats that captures fibrin fibrils and fibrinogen. Pathogenic staphylococci express several different SD proteins that are modified by two glycosyltransferases, SdgA and SdgB. Here, we characterized three genes of S. aureus, aggA, aggB (sdgA), and aggC (sdgB), and show that aggA and aggC contribute to staphylococcal agglutination with fibrin fibrils in human plasma. We demonstrate that aggB (sdgA) and aggC (sdgB) are involved in GlcNAc modification of the ClfA SD repeats. However, only sdgB is essential for GlcNAc modification, and an sdgB mutant is defective in the pathogenesis of sepsis in mice. Thus, GlcNAc modification of proteins promotes S. aureus replication in the bloodstream of mammalian hosts.
Highlights
Staphylococcus aureus agglutinates in plasma in a manner that requires host fibrinogen and clumping factor A, a bacterial surface protein with serine-aspartate (SD) repeats
In Gram-negative microbes, oligosaccharyltransferase appears to utilize undecaprenyl-linked carbohydrates that are transferred onto secreted proteins in the bacterial periplasm [36]
For several Gram-positive bacteria, O-linked glycosylation targets polypeptides that require their carbohydrate modification as a prerequisite for their entry into dedicated secretion pathways, which may culminate in assembly of adhesive molecules on microbial surfaces or in murein hydrolase function [39, 40]
Summary
Staphylococcus aureus agglutinates in plasma in a manner that requires host fibrinogen and clumping factor A, a bacterial surface protein with serine-aspartate (SD) repeats. The agglutination reaction involves ClfA (clumping factor A), a surface protein with serine-aspartate (SD) repeats that captures fibrin fibrils and fibrinogen. We characterized three genes of S. aureus, aggA, aggB (sdgA), and aggC (sdgB), and show that aggA and aggC contribute to staphylococcal agglutination with fibrin fibrils in human plasma. Staphylococcus aureus is the most frequent cause of human bloodstream infection, sepsis, and endocarditis in the United States [1, 2] This Gram-positive bacterium evolved to clot animal and human plasma, bind fibrinogen, and agglutinate within a meshwork of fibrin fibrils [3]. S. aureus aggC (sdgB) variants, but not aggB (sdgA) variants, are defective in the pathogenesis of bloodstream infections in mice
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