Effect of Anti-bacterial Molecules on Streptococcus gordonii Adhesion Gene Expression

Objectives: In the oral cavity, bacterial adhesion to surfaces is necessary for survival. We hypothesized that Streptococcus gordonii (Sg), an oral bacterium, could sense anti-bacterial molecules and alter adhesin gene expression to maintain adhesion. We hypothesized that as anti-bacterial molecules, human neutrophil-peptide (HNP-1) signaling through the Sg histidine kinase (HK), SGO_1180, the homolog of Staphylococcus aureus SaeS HK, and Ig targeting SspA/SspB (P1) would activate downstream genes including adhesins.
Methods: Sg was grown overnight in BHI broth. Anti-bacterial molecules tested were HNP-1 and IgG specific for the adhesins, SspA/SspB (P1). To sense HNP-1, the transmembrane domain linker of SGO_1180 was replaced with the SaeS linker. Cells were lysed, RNA extracted and used as template for cDNA synthesis, and expression was measured using RT-qPCR. The RT-qPCR data was analyzed using the △△CT method. Biofilm production was assayed by crystal-violet release from cells attached to plastic.
Results: Response to HNP-1: Biofilm production was reduced in the presence of HNP-1, but our data suggest that SGO_1180/SaeS HKs do not sense HNP-1, contrary to published reports.
Response to anti-P1 antibody: In response to anti-P1, sspA and sspB expression decreased two-fold. Interestingly, expression of sgo_0707 adhesin also decreased two-fold while the expression of the adhesin, scaA, remained unchanged. Our data indicate that Sg selectively alters adhesin expression in response to specific Ig; the global effect on adhesin expression remains to be determined.
Conclusions: These data suggest that Sg biofilm formation is negatively impacted by HNP-1, but in an SGO_1180/SaeS independent manner. Further, Sg alters adhesin expression in response to specific anti-adhesin antibody. These data suggest that Sg regulates adhesin expression in response to anti-bacterial molecules to favor persistence in the oral cavity.