TY - JOUR
T1 - Role of the Streptococcus mutans gtf Genes in Caries Induction in the Specific-Pathogen-Free Rat Model
AU - Yamashita, Y.
AU - Bowen, W. H.
AU - Burne, R. A.
AU - Kuramitsu, H. K.
N1 - Funding Information:
This investigation was supported in part by grants DE03258 (H.K.K.) and DE07003 (W.H.B.) from the National Institutes of Health.
Publisher Copyright:
Copyright © 1993, American Society for Microbiology
PY - 1993/9
Y1 - 1993/9
N2 - The role of each of the Streptococcus mutans gtf genes coding for glucan synthesis in cariogenesis was evaluated by using strain UA130 in the specific-pathogen-free (SPF) rat model system. Mutants defective in either or both of the genes required for insoluble glucan synthesis, the gtfB and gtfC genes, exhibited markedly reduced levels of smooth-surface carious lesions relative to that of the parental organism. Likewise, the mutant defective in the gtfD gene coding for the glucosyltransferase-S enzyme synthesizing water-soluble glucans also produced significantly fewer smooth-surface lesions than strain UA130. None of these mutations markedly altered the rate of sulcal caries induction relative to that of the parental organism. In addition, a mutant of strain UA130 defective in the gtf A gene was reexamined in the SPF rat model. In contrast to previous results from a gnotobiotic rat system, these mutants also induced significantly fewer smooth-surface carious lesions compared with that by strain UA130. These results suggest that all four genes are important for smooth-surface caries formation. Furthermore, these results are discussed relative to the differences in the diets utilized in the SPF and gnotobiotic rat model systems for assessing the virulence factors of 5. mutans.
AB - The role of each of the Streptococcus mutans gtf genes coding for glucan synthesis in cariogenesis was evaluated by using strain UA130 in the specific-pathogen-free (SPF) rat model system. Mutants defective in either or both of the genes required for insoluble glucan synthesis, the gtfB and gtfC genes, exhibited markedly reduced levels of smooth-surface carious lesions relative to that of the parental organism. Likewise, the mutant defective in the gtfD gene coding for the glucosyltransferase-S enzyme synthesizing water-soluble glucans also produced significantly fewer smooth-surface lesions than strain UA130. None of these mutations markedly altered the rate of sulcal caries induction relative to that of the parental organism. In addition, a mutant of strain UA130 defective in the gtf A gene was reexamined in the SPF rat model. In contrast to previous results from a gnotobiotic rat system, these mutants also induced significantly fewer smooth-surface carious lesions compared with that by strain UA130. These results suggest that all four genes are important for smooth-surface caries formation. Furthermore, these results are discussed relative to the differences in the diets utilized in the SPF and gnotobiotic rat model systems for assessing the virulence factors of 5. mutans.
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U2 - 10.1128/iai.61.9.3811-3817.1993
DO - 10.1128/iai.61.9.3811-3817.1993
M3 - Article
C2 - 8359902
AN - SCOPUS:0027323903
VL - 61
SP - 3811
EP - 3817
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 9
ER -
