Streptococcus mutans: Fructose Transport, Xylitol Resistance, and Virulence

Abstract

Streptococcus mutans, the primary etiological agent of human dental caries, possesses at least two fructose phosphotransferase systems (PTSs), encoded by fruI and fruCD. fruI is also responsible for xylitol transport. We hypothesized that fructose and xylitol transport systems do not affect virulence. Thus, colonization and cariogenicity of fruI − and fruCD − single and double mutants, their WT (UA159), and xylitol resistance (X r ) of S. mutans were studied in rats fed a high-sucrose diet. A sucrose phosphorylase (gtfA − ) mutant and a reference strain (NCTC-10449S) were additional controls. Recoveries of fruI mutant from the teeth were decreased, unlike those for the other strains. The fruCD mutation was associated with a slight loss of cariogenicity on enamel, whereas mutation of fruI was associated with a loss of cariogenicity in dentin. These results also suggest why xylitol inhibition of caries is paradoxically associated with spontaneous emergence of so-called X r S. mutans in habitual human xylitol users.

Salivary Mucin 19 Glycoproteins

“…The gtfA gene does not alter carbohydrate metabolism of S. mutans, except for melibiose and raffinose (33). Caries development by this strain is unaffected (34), and collected saliva produced no colonies under anaerobic conditions on blood agar containing 1 mg/ml kanamycin (data not shown).…”

Point-of-care salivary microbial tests for detection of cariogenic species — Clinical relevance thereof — review

“…group are capable of rapid uptake of sucrose in competition with other plaque bacteria through several transport systems such as phosphoenolpyruvate-dependent, fructose-specific, phosphotransferase systems (Tanzer et al 2006). These bacteria synthesize insoluble extracellular polysaccharides (homopolymers glucans, fructans, mutams and dextrans) mediated by glucosyltransferases and fructosyltransferase, which contribute to the co-aggregation of bacteria within the plaque matrix (Loesche 1986), but despite previous assumptions they probably do not represent a significant mechanism of initial colonization of tooth surface, as mutans streptococci comprise only 2 % or less of the initial streptococcal microflora irrespective of individual exposure to sucrose (Nyvad and Kilian 1987) and a number of protein adhesins that can interact with salivary molecules and favor colonization and interbacterial co-aggregation (Love and Jenkinson 2002; Sato et al 1997).…”

Risk Indicators of Pre-Eclampsia in North Jordan: Is Dental Caries Involved?

“…Streptococcus mutans is the primary etiological agent of human dental caries [18] . Interestingly, pre-eclampsia is now known to have an underlying inflammatory basis with activation of circulating leukocytes and altered levels of inflammatory cytokines [19] , and there is an emerging role of C-reactive protein testing in managing this OR = Unadjusted odds ratios; CI = confidence interval.…”