Comparison of genes required for H₂O₂ resistance in Streptococcus gordonii and Streptococcus sanguinis

Hydrogen peroxide (H₂O₂) is produced by several members of the genus Streptococcus mainly through the pyruvate oxidase SpxB under aerobic growth conditions. The acute toxic nature of H₂O₂ raises the interesting question of how streptococci cope with intrinsically produced H₂O₂, which subsequently accumulates in the microenvironment and threatens the closely surrounding population. Here, we investigate the H₂O₂ susceptibility of oral Streptococcus gordonii and Streptococcus sanguinis and elucidate potential mechanisms of how they protect themselves from the deleterious effect of H₂O₂. Both organisms are considered primary colonizers and occupy the same intraoral niche making them potential targets for H₂O₂ produced by other species. We demonstrate that S. gordonii produces relatively more H₂O₂ and has a greater ability for resistance to H₂O₂ stress. Functional studies show that, unlike in Streptococcus pneumoniae, H₂O₂ resistance is not dependent on a functional SpxB and confirms the important role of the ferritin-like DNA-binding protein Dps. However, the observed increased H₂O₂ resistance of S. gordonii over S. sanguinis is likely to be caused by an oxidative stress protection machinery present even under anaerobic conditions, while S. sanguinis requires a longer period of time for adaptation. The ability to produce more H₂O₂ and be more resistant to H₂O₂ might aid S. gordonii in the competitive oral biofilm environment, since it is lower in abundance yet manages to survive quite efficiently in the oral biofilm.