‘Disease-State’ Salivary Metabolome Changes Disrupt Multispecies Oral Biofilms

Objectives: Numerous studies have considered saliva as a key host sample for identifying noninvasive disease biomarkers. Both pancreatic cancer and renal disease have documented shifts in the oral microbiome and a number of host salivary metabolome products. However, these studies have not looked at potential links between the detected shifts. One hypothesis for the observed shifts seen in the oral microbiome is disruption of bacterial growth and adhesion in direct response to a change in host saliva metabolic products. In the present work, two salivary metabolome analysts, glutamine and phosphate, were compared for their ability to influence the biofilm formation of a multispecies oral model with Lactobacillus casei, Streptococcus gordonii, Actinomyces oris, and Streptoccocus mutans.
Methods: Biofilm formation was observed in the presence of sterile ‘healthy’ saliva or ‘disease-state’ saliva, supplemented with phosphate or glutamine consistent with renal failure or pancreatic cancer, respectively. The resulting biofilms, performed in quadruplet or greater for each condition, were examined for structure, thickness, and coverage by confocal laser scanning microscopy using Live/Dead staining.
Results: Elevated glutamine or phosphate levels consistent with ‘disease-states’ in the saliva were both shown to be effective in impairing bacterial adhesion and formation of multi-species biofilms. Biofilm three dimensional architecture was completely disrupted, resulting in a monolayer, in the presence of elevated phosphate, while elevated salivary glutamine levels showed a significant decrease in biofilm thickness and major disruption of biofilm structure. Low levels of metabolites in 50% diluted ‘heathy’ saliva resulted in a similar overall biofilm arrangement to the non-diluted saliva but showed a reduction in biofilm thickness.
Conclusions: All together, these data imply that specific shifts in the host salivary metabolome can directly influence adhesion and biofilm architecture of a multispecies model providing a potential mechanism for the observed shift in the oral microbiome in response to a systemic disease state.