Adhesion of viridans group streptococci to sialic acid‐, galactose‐ and N‐acetylgalactosamine‐containing receptors

Abstract

The binding of 10 viridans group streptococci to sialic acid-, galactose (Gal)- and N-acetylgalactosamine (GalNAc)-containing receptors was defined by analysis of the interactions between these bacteria and structurally defined glycoconjugates, host cells and other streptococci. All interactions with sialic acid-containing receptors were Ca(2+)-independent as they were not affected by ethyleneglycoltetraacetic acid (EGTA), whereas all interactions with Gal- and GalNAc-containing receptors were Ca(2+)-dependent. Recognition of sialic acid-, Gal- and GalNAc-containing receptors varied widely among the strains examined, in a manner consistent with the association of each of the three lectin-like activities with a different bacterial cell surface component.

A C-Type Lectin MGL1/CD301a Plays an Anti-Inflammatory Role in Murine Experimental Colitis

“…35 Coaggregation of Streptococcus viridans, a member of the oral flora, was inhibited by the addition of oligosaccharides containing Gal and/or GalNAc, 36 strongly suggesting that Gal/GalNAc residues were exposed on the surfaces of Streptococci. Another study showed that Gal and GalNAc residues were present in an exo-polysaccharide or a capsular polysaccharide produced by Lactobacillus.…”

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

“…Bacterial strains and growth conditions: The S. gordonii strains used in this study included DL1 (Challis strain, wild type, biovar 2) (12,22) and its hsa mutant EM230 (DL1 hsa::ermAM) (8) as well as several other wild-type S. gordonii strains, including 38, SK6 (biovar 1), M5, 10558 (biovar 2), and SK12 (biovar 3) (12,22). All streptococci were cultured overnight in brain-heart infusion broth (Difco, Becton-Dickinson and Company, Sparks, MD, USA) at 37 C. The medium was supplemented with 10 µg mL of erythromycin (Sigma-Aldrich, St. Louis, MO, USA) as needed.…”

“…Host sialic acid-containing receptors for Hsa adhesin include the salivary mucin MG2 (11,12), leukosialin (CD43) (13), platelet glycoprotein Ibα (14), erythrocyte glycophorin A and band3 (15), and leukocyte CD11b and CD50 (16). 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).…”

Identification of Platelet Receptors for the Streptococcus gordonii DL1 Sialic Acid‐Binding Adhesin

“…We have previously identified and functionally characterized the gene (hsa) encoding the sialic acidbinding adhesin (Hsa) of S. gordonii DL1, a glycoprotein containing GlcNAc (24,25,27). Hsa binds α2-3-linked sialic acid termini of O-glycosylated mucin-type glycoproteins, including salivary mucin MG2 and leukosialin, the major surface glycoprotein of human polymorphonuclear leukocytes (20,21,(24)(25)(26).…”

“…We have previously identified and functionally characterized the gene (hsa) encoding the sialic acidbinding adhesin (Hsa) of S. gordonii DL1, a glycoprotein containing GlcNAc (24,25,27). Hsa binds α2-3-linked sialic acid termini of O-glycosylated mucin-type glycoproteins, including salivary mucin MG2 and leukosialin, the major surface glycoprotein of human polymorphonuclear leukocytes (20,21,(24)(25)(26).We have also shown that the aggregation of human platelets by S. gordonii DL1, an interaction implicated in the pathogenesis of infective endocarditis (11), required the expression of hsa (27). In addition, neuraminidase-treatment of the platelets abolished this interaction, further supporting the essential role of Hsa in the bacteria-platelet interaction (27).…”