Abstract
Streptococcus mutans, a cariogenic bacterium in humans, is associated with systemic disorders. Its cariogenic factors include glucosyltransferases (GTFs) and the glycosyltransferase rhamnose-glucose polysaccharide I (RgpI), which is involved in cell wall synthesis. However, the potential roles of these enzymes in systemic disorders remain unclear. We constructed a luciferase-tagged S. mutans UA159 mutant strain that lacked rgpI to explore the involvement of this enzyme in the systemic pathogenicity of S. mutans. We also employed the luciferase-tagged S. mutans UA159 variant, which exhibited reduced GTF production and therefore had a low glucan synthesis ability. We intravenously inoculated these luciferase-tagged mutants and parent strains into 12-week-old male BALB/c mice to evaluate their distribution to organs. Strong luminescence was noted in the spleen and kidneys, indicating that S. mutans was disseminated to these organs. Several organs collected from mice inoculated with the luciferase-tagged parent strain emitted a signal, and inflammatory cytokine production was detected in the blood. The luminescence intensity was lower in the kidneys of mice challenged with the mutant strain, which has a low glucan synthesis ability. Conversely, challenge with the rgpI deletion mutant strain resulted in the lowest number of luminescent organs, with a lower intensity and attenuated inflammation. Furthermore, all the mice inoculated with the rgpI deletion mutant strain survived, whereas not all the mice inoculated with the parent strain survived. Collectively, these results suggest that RgpI is involved in the systemic pathogenicity of S. mutans UA159.