Streptococcus mutansAdherence: Presumptive Evidence for Protein-Mediated Attachment Followed by Glucan-Dependent Cellular Accumulation

Autor: Staat, Robert H., Langley, Sharon D., Doyle, R. J.
Zdroj: Infection and Immunity; February 1980, Vol. 27 Issue: 2 p675-681, 7p
Abstrakt: Adherence of Streptococcus mutansto smooth surfaces has been attributed to the production of sucrose-derived d-glucans. However, several studies indicate that the bacterium will adhere in the absence of sucrose. The present data confirmed that S. mutansadherence to saliva-coated hydroxyapatite beads in the absence of sucrose is described by the Langmuir equation. The nature of the sucrose-independent adherence was studied with the Persea americanaagglutinin as a selective adherence inhibitor. Pretreatment of the bacterium with P. americanaagglutinin caused a 10-fold reduction in adherence, and the inhibition was not reversed with the addition of sucrose. Pretreatment of S. mutanswith proteases also reduced adherence, regardless of the sucrose content, whereas periodate oxidation and glucanohydrolase treatment of the bacteria reduced sucrose-mediated adherence to the levels found for sucrose-independent adherence. The P. americanaagglutinin, glucanohydrolase, and pepsin pretreatment of the cells did not eliminate sucrose-induced agglutination. Scanning electron microscopy showed that short streptococcal chains were bound to saliva-coated hydroxyapatite crystals in the sucrose-independent system, whereas the presence of sucrose caused larger bacterial clumps to be found. A two-reaction model of S. mutansadherence was developed from these data. It is proposed that one reaction is attachment to the tooth pellicle which is mediated by cell-surface proteins rather than glucans or teichoic acids. The other reaction is cellular accumulation mediated by sucrose-derived d-glucans and cell surface lectins. A series of sequential adherence experiments with P. americanaagglutinin as a selective inhibitor provided presumptive evidence for the validity of our model of S. mutansadherence.
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