Alkali production associated with malolactic fermentation by oral streptococci and protection against acid, oxidative, or starvation damage. Sheng Jiangyun,Baldeck Jeremiah D,Nguyen Phuong T M,Quivey Robert G,Marquis Robert E Canadian journal of microbiology Alkali production by oral streptococci is considered important for dental plaque ecology and caries moderation. Recently, malolactic fermentation (MLF) was identified as a major system for alkali production by oral streptococci, including Streptococcus mutans. Our major objectives in the work described in this paper were to further define the physiology and genetics of MLF of oral streptococci and its roles in protection against metabolic stress damage. L-Malic acid was rapidly fermented to L-lactic acid and CO(2) by induced cells of wild-type S. mutans, but not by deletion mutants for mleS (malolactic enzyme) or mleP (malate permease). Mutants for mleR (the contiguous regulator gene) had intermediate capacities for MLF. Loss of capacity to catalyze MLF resulted in loss of capacity for protection against lethal acidification. MLF was also found to be protective against oxidative and starvation damage. The capacity of S. mutans to produce alkali from malate was greater than its capacity to produce acid from glycolysis at low pH values of 4 or 5. MLF acted additively with the arginine deiminase system for alkali production by Streptococcus sanguinis, but not with urease of Streptococcus salivarius. Malolactic fermentation is clearly a major process for alkali generation by oral streptococci and for protection against environmental stresses. 10.1139/w10-039

D‑Tagatose inhibits the growth and biofilm formation of Streptococcus mutans. Hasibul Khaleque,Nakayama-Imaohji Haruyuki,Hashimoto Masahito,Yamasaki Hisashi,Ogawa Takaaki,Waki Junpei,Tada Ayano,Yoneda Saori,Tokuda Masaaki,Miyake Minoru,Kuwahara Tomomi Molecular medicine reports Dental caries is an important global health concern and Streptococcus mutans has been established as a major cariogenic bacterial species. Reports indicate that a rare sugar, D‑tagatose, is not easily catabolized by pathogenic bacteria. In the present study, the inhibitory effects of D‑tagatose on the growth and biofilm formation of S. mutans GS‑5 were examined. Monitoring S. mutans growth over a 24 h period revealed that D‑tagatose prolonged the lag phase without interfering with the final cell yield. This growth retardation was also observed in the presence of 1% sucrose, although it was abolished by the addition of D‑fructose. S. mutans biofilm formation was significantly inhibited by growth in sucrose media supplemented with 1 and 4% D‑tagatose compared with that in a culture containing sucrose alone, while S. mutans formed granular biofilms in the presence of this rare sugar. The inhibitory effect of D‑tagatose on S. mutans biofilm formation was significantly more evident than that of xylitol. Growth in sucrose media supplemented with D‑tagatose significantly decreased the expression of glucosyltransferase, exo‑β‑fructosidase and D‑fructose‑specific phosphotransferase genes but not the expression of fructosyltransferase compared with the culture containing sucrose only. The activity of cell‑associated glucosyltransferase in S. mutans was inhibited by 4% D‑tagatose. These results indicate that D‑tagatose reduces water‑insoluble glucan production from sucrose by inhibiting glucosyltransferase activities, which limits access to the free D‑fructose released during this process and retards the growth of S. mutans. Therefore, foods and oral care products containing D‑tagatose are anticipated to reduce the risk of caries by inhibiting S. mutans biofilm formation. 10.3892/mmr.2017.8017