title: Defect of glucosyltransferases reduces platelet aggregation activity of Streptococcus mutans: analysis of clinical strains isolated from oral cavities.
abstract: OBJECTIVE
  Streptococcus mutans is a major pathogen of dental caries and occasionally isolated from the blood of patients with infective endocarditis, though the association of its cell-surface glucosyltransferases (GTFB, GTFC, and GTFD) with pathogenicity for infective endocarditis remains to be elucidated. In this study, we investigated the contribution of S. mutans GTFs to platelet aggregation and analysed GTF expression profiles in a large number of clinical oral isolates.
  
  
  METHODS
  The platelet aggregation properties of GTF-defective isogenic mutant strains constructed from S. mutans reference strain MT8148 were evaluated using whole blood and platelet-rich plasma (PRP) taken from mice, as well as human PRP. In addition, GTF expression profiles for 396 S. mutans strains isolated from the oral cavities of 396 subjects were analysed by western blotting using antisera specific for each GTF.
  
  
  RESULTS
  The platelet aggregation activities of the GTF-defective isogenic mutants were significantly lower than that of MT8148 when added to a large number of cells. Western blotting revealed no strains without GTF expression, though six strains had alterations of GTFB and GTFC as compared to MT8148. PCR analyses indicated that the gtfB-gtfC region length was approximately 4.5 kb shorter in those strains as compared to MT8148. These were designated as "GTFBC-fusion" strains and they demonstrated lower levels of platelet aggregation.
  
  
  CONCLUSIONS
  Our findings indicate that GTFs are associated with platelet aggregation. Although the clinical detection frequency of S. mutans strains with altered expressions is extremely low, GTFBC-fusion strains have activities similar to GTF-defective mutant strains.
authors.affiliation: Department of Pediatric Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Taniguchi
authors.forename: K
authors.initials: K
authors.lastname: Nakano
authors.forename: R
authors.initials: R
authors.lastname: Nomura
authors.forename: S
authors.initials: S
authors.lastname: Naka
authors.forename: A
authors.initials: A
authors.lastname: Kojima
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
authors.forename: T
authors.initials: T
authors.lastname: Ooshima
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000818:Animals; D001769:Blood / Q000382:microbiology; D015870:Gene Expression; D016695:Glycosyltransferases / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics; D006801:Humans; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009055:Mouth / Q000382:microbiology; D010974:Platelet Aggregation; D053657:Platelet-Rich Plasma / Q000382:microbiology; D013045:Species Specificity; D013295:Streptococcus mutans / Q000201:enzymology* / Q000502:physiology
chemical_list: D016695:Glycosyltransferases