Streptococcal Antagonism in Oral Biofilms

Oral biofilms are polymicrobial and the diverse bacterial species compete for the limited space and nutrients. Under healthy conditions, the different species in the oral biofilms maintain an ecological balance. This balance can be disturbed by environmental and biological factors, leading to dominant growth of certain species associated with disease. How these changes occur on the molecular level is not well understood. In this study, we used three well-characterized members of oral biofilms, Streptococcus mutans, Streptococcus sanguinis and Streptococcus gordonii, to model clinically relevant streptococcal antagonism that could lead to caries development. Objective: To learn how the environmental oxygen and nutritional glucose influence the virulence properties and competition between oral streptococci. Methods: Competition studies were used to monitor the antagonism between the streptococci under different conditions. Isogenic pyruvate oxidase mutants were constructed to asses the role of hydrogen-peroxide (H₂O₂) in the competition. H₂O₂ production was measured for S. gordonii and S. sanguinis. Furthermore, the expression of S. mutans competence and bacteriocin genes was determined with real-time RT PCR under aerobic and anaerobic conditions. The release of heterologous DNA was measured in mixed cultures with and without oxygen. Results: Oxygen and glucose availability affected H₂O₂ production by S. gordonii and S. sanguinis, but did not affect virulence of S. mutans. Furthermore, aerobic conditions favored expression of the competence and bacteriocin genes of S. mutans, correlating with an increase of pyruvate oxidase-dependent DNA release from the other streptococci. Conclusion: Environmental oxygen and nutritional glucose substantially influenced the competitiveness of the tested species of streptococci. As a consequence, S. mutans might increase in numbers when the diet is glucose-rich, even in the absence of sucrose, and initiate the development of caries.

NIH/NIDCR R01 DE8590 to M.C.H. and 1K99DE018400-01 to J.K.