Host collagen signal induces antigen I/II adhesin and invasin gene expression in oral Streptococcus gordonii

Abstract

SummaryMicrobial interactions with host molecules, and programmed responses to host environmental stimuli, are critical for colonization and initiation of pathogenesis. Bacteria of the genus Streptococcus are primary colonizers of the human mouth. They express multiple cell-surface adhesins that bind salivary components and other oral bacteria and enable the development of polymicrobial biofilms associated with tooth decay and periodontal disease. However, the mechanisms by which streptococci invade dentine to infect the tooth pulp and periapical tissues are poorly understood. Here we show that production of the antigen I/ II (AgI/II) family polypeptide adhesin and invasin SspA in Streptococcus gordonii is specifically upregulated in response to a collagen type I signal, minimally the tri-peptide Gly-Pro-Xaa (where Xaa is hydroxyproline or alanine). Increased AgI/II polypeptide expression promotes bacterial adhesion and extended growth of streptococcal cell chains along collagen type I fibrils that are characteristically found within dentinal tubules. These observations define a new model of host matrix signal-induced tissue penetration by bacteria and open the way for novel therapy opportunities for oral invasive diseases.

Streptococcus pyogenes Collagen Type I-binding Cpa Surface Protein

“…Most interestingly, there was no consistent evidence for enhanced cpa expression in the presence of collagen type I peptide fragments as seen in other streptococcal species (44,83,84). However, the presence of collagen peptides did influence expression of two S. pyogenes regulatory genes, mga and nra.…”

Streptococcus gordonii Modulates Candida albicans Biofilm Formation through Intergeneric Communication

“…The strains of microorganisms used were S. gordonii wild-type strain DL1 (Challis), S. gordonii UB1360 ⌬(sspA sspB) (24), S. gordonii UB1545 ⌬hsa (36), an S. gordonii ⌬luxS mutant, a ⌬luxS::luxS ϩ complemented strain (48), P. aeruginosa PAO1, and C. albicans SC5314. S. gordonii was cultivated on BHY agar (37 g/liter brain heart infusion broth, 5 g/liter yeast extract, 15 g/liter agar) anaerobically, P. aeruginosa was cultivated on tryptic soy agar aerobically, and C. albicans was cultivated on Sabouraud dextrose agar (Oxoid) aerobically; all cultures were incubated at 37°C.…”

“…Some of these polypeptides, the conserved antigen I/II (AgI/II) family of cell wall-anchored proteins, which range from 826 to 1,653 amino acid residues long, are produced by most indigenous oral Streptococcus species (32,55). These proteins recognize a range of host tissue proteins and cellular receptors (24,30,31,36), in addition to mediating binding to specific partner microorganisms (e.g., Actinomyces naeslundii, Porphyromonas gingivalis, and Candida albicans) (13,16,28,45).…”

Platelet-Bacterial Interactions in the Pathogenesis of Infective Endocarditis — Part I: The Streptococcus

“…SspA and SspB participate in fluid phase interactions with salivary glycoprotein gp340, facilitating bacterial clumping which most likely aids in the development of biofilms [59,60]. Additionally, they mediate adherence and internalisation into epithelial cells via β1 intregins [57], can bind to collagen type 1 [61] and interact with other oral microorganisms: Candida albicans [62]; Porphyromonas gingivalis [63]; and Actinomyces naeslundii [60]. Given their critical role in induction of platelet aggregation it is tempting to speculate that S. gordonii strains lacking antigen I/II proteins may have reduced virulence in IE due to failure to propagate platelet activation.…”