Effect of human saliva on glucose uptake by Streptococcus mutans and other oral microorganisms.
We examined the effects of human whole salivary supernatant and parotid fluid on glucose uptake by Streptococcus mutans, Streptococcus sanguis, Streptococcus mitis, Actinomyces viscosus, Staphylococcus aureus, and Escherichia coli. The following three effects of saliva were observed: (i) inhibition of glucose uptake (S. mutans, S. sanguis), (ii) promotion of a transient, rapid (0 to 30 s) burst of glucose uptake (S. mutans, S. sanguis), and (iii) enhancement of glucose uptake (S. mitis, A. viscosus, S. aureus, E. coli). We observed no differences between the effects of whole salivary supernatant and the effects of parotid fluid. Heat treatment (80 degrees C, 10 min) of saliva or the addition of dithiothreitol abolished inhibition of glucose uptake. Supplementation of saliva with H(2)O(2) potentiated inhibition of glucose uptake. S. mitis and A. viscosus, which were stimulated by saliva alone, were inhibited by H(2)O(2)-supplemented saliva; 50% inhibition of glucose uptake by S. mutans and S. mitis required ca. 10 muM H(2)O(2) in 50% (vol/vol) saliva. Loss of the inhibitory action of saliva occurred at about 5% (vol/vol) saliva. Supplementation of saliva dilutions with SCN(-) and H(2)O(2) extended the inhibitory activity to solutions containing ca. 0.2% (vol/vol) saliva. We suggest that the salivary lactoperoxidase-SCN(-)-H(2)O(2) system is responsible for the inhibitory activity of saliva reported here. Furthermore, we concluded that lactoperoxidase and SCN(-) are present in saliva specimens in concentrations that exceed minimal inhibitory levels by factors of ca. 500 and 10 to 20, respectively. The resistance of A. viscosus, S. aureus, and E. coli to the inhibitory potential of saliva alone was probably due to the production of catalase by these organisms. The resistance of S. mitis may have been due to special effects of saliva on H(2)O(2) accumulation by this organism compared with S. mutans and S. sanguis. The basis of saliva-dependent enhancement of glucose uptake and the basis of promotion of a transient, rapid burst of glucose uptake are unknown. The role of the salivary lactoperoxidase-SCN(-)-H(2)O(2) system in the oral microbial ecosystem is discussed.
D000190:Actinomyces / Q000378:metabolism; D004229:Dithiothreitol / Q000494:pharmacology; D004926:Escherichia coli / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006358:Hot Temperature; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D009055:Mouth / Q000382:microbiology*; D010306:Parotid Gland; D012463:Saliva / Q000382:microbiology / Q000502:physiology*; D013211:Staphylococcus aureus / Q000378:metabolism; D013291:Streptococcus / Q000378:metabolism; D013295:Streptococcus mutans / Q000378:metabolism*
D006861:Hydrogen Peroxide; D005947:Glucose; D004229:Dithiothreitol