Contribution of Sialic Acid-Binding Adhesin to Pathogenesis of Experimental Endocarditis Caused by Streptococcus gordonii DL1

Abstract

An insertional mutation in hsa, the gene encoding the sialic acid-binding adhesin of Streptococcus gordonii DL1, resulted in a significant reduction of the infection rate of the organism and an inflammatory reaction in the rat aortic valve with experimental endocarditis, suggesting that the adhesin contributes to the infectivity of the organism for heart valves.

Glycine Residues in the Hydrophobic Core of the GspB Signal Sequence Route Export toward the Accessory Sec Pathway

“…Although identified only relatively recently, in part because of their extremely high apparent molecular mass and failure to react with conventional protein stains, these glycoproteins have been found not only to bind specific receptors on human tissues (7,35,45,47,48,57) but also to contribute to virulence, as measured by animal models of infection (32,40,42,46).…”

“…This unusual adhesin is a member of an expanding family of serine-rich glycoproteins which includes Fap1 of Streptococcus parasanguinis, Hsa of S. gordonii Challis, SraP of Staphylococcus aureus, the Srr proteins of Streptococcus agalactiae, and the SrpA proteins of Streptococcus sanguinis and Streptococcus cristatus (21,35,40,42,44,56). Although identified only relatively recently, in part because of their extremely high apparent molecular mass and failure to react with conventional protein stains, these glycoproteins have been found not only to bind specific receptors on human tissues (7,35,45,47,48,57) but also to contribute to virulence, as measured by animal models of infection (32,40,42,46).…”

Contribution of <i>Streptococcus gordonii</i> Hsa Adhesin to Biofilm Formation

“…The Hsa adhesin and its homologs facilitate attachment of S. gordonii to host cells, such as polymorphonuclear leukocytes (13,16), erythrocytes (7,15), platelets (9,14,17,18), macrophages, and monocytes (19). In addition, Hsa adhesin contributes to the pathogenesis of experimental infectious endocarditis caused by S. gordonii DL1 (6). Moreover, the results of our recent study suggested that monocytes stimulated with S. gordonii DL1 rapidly differentiate into dendritic cells through interactions with Hsa (19).…”

“…Thus, these bacteria are members of the biofilm community on teeth known as dental plaque, and are associated with the pathogenesis of dental caries and periodontal disease (1)(2)(3). These bacteria are also known to colonize damaged heart valves, and are considered to be an important causative agent of infective endocarditis (4)(5)(6).…”

Infective Endocarditis

“…Other proposed virulence factors that mediate streptococcal adhesion include FimA, which is a surface protein that functions as an adhesin in the oral cavity 43,44 , the sialic acid-binding adhesin Hsa 45 and a phage-encoded bacterial adhesin that mediates a complex interaction between bacteria, fibrinogen and platelets [46][47][48] .…”