ライフサイエンスコーパス: S. mutans

1 S. mutans catabolizes both glucose and sucrose, producin

2 S. mutans cells subjected to mechanical extraction were

3 S. mutans DNA, plaque area, inflammatory cell invasion,

4 S. mutans genomic DNA was detected in the aorta, liver,

5 S. mutans grown with sucrose in the presence of Streptoc

6 S. mutans may also be associated with atherosclerotic pl

7 S. mutans may not act alone; Candida albicans cells are

8 S. mutans out-competed S. gordonii in in vivo plaque bio

9 S. mutans preferentially consumed sucrose in a mixed die

10 S. mutans SRP pathway mutants demonstrate growth defects

11 S. mutans strains lacking a functional Fpg, MutY or Smn

12 S. mutans UA159, a sequenced strain, produces at least t

13 S. mutans-positive children had higher food cariogenicit

14 A S. mutans biofilm model in acidic and neutral medium was

15 through heterologous expression of gacA in a S. mutans rmlD knockout, which restored attenuated growt

16 within microcolonies which in turn activates S. mutans acid-stress response, mediating both the local

17 study was to examine whether nitrite affects S. mutans virulence during polymicrobial infections with

18 ton has remarkably specific activity against S. mutans, causing acid-mediated cell death during biofi

19 ommensal, has antimicrobial activity against S. mutans.

20 vely influenced in antagonism assays against S. mutans.

21 antibacterial activity was observed against S. mutans at lower pH (6.4).

22 PDT (660-nm light) was carried out against S. mutans biofilms grown on either plastic dishes or on

23 cocci and nitrite provide protection against S. mutans pathogenesis.

24 effect of SeLECT-Defense(TM) sealant against S. mutans and S. salivarius biofilms is very effective a

25 rmation) demonstrate Muc19 poorly aggregates S. mutans.

26 ariogenesis, the possible coordination among S. mutans' main virulence factors, including glucan prod

27 An S. mutans affinity column was used to isolate active moi

28 tly promoted by subjecting all samples to an S. mutans acidic biofilm for 6 d.

29 mutans with bifidobacteria (p < 0.001), and S. mutans with S. wiggsiae (p = 0.001).

30 nd amylase-binding proteins (AbpA/AbpB), and S. mutans glucosyltransferase (GtfB), affect their respe

31 -dependent synergism between C. albicans and S. mutans contribute to enhanced pathogenesis.

32 iofilm removal from machine-etched glass and S. mutans from typodont surfaces with complex topography

33 While both S. gordonii and S. mutans were abundant colonizers of rat's teeth in the

34 n failed to inhibit the activity of Gtfs and S. mutans biofilms, signifying the specificity of the le

35 atum subspecies animalis and polymorphum and S. mutans non-c serotypes, are prone to extra-oral trans

36 iate modeling employing HOT, S. sobrinus and S. mutans (PCR/qPCR), and sugar snacks separated Romania

37 that the LTF/K variant results in both anti-S. mutans activity and reduced decay.

38 at KK subjects were more likely to have anti-S. mutans activity than RR subjects (P = 0.001; relative

39 potential of structure-based design of anti-S. mutans virulence inhibitors.

40 was to identify a salivary protein with anti-S. mutans activity, characterize its genotype, and deter

41 suggested that this proton enrichment around S. mutans could pre-condition the bacterium for acid-str

42 The UAS was also highly effective at S. mutans, A. naeslundii, and S. oralis biofilm removal

43 d/or enzymatic activity, cooperation between S. mutans strains or with other members of the oral biot

44 Here, we examined the binding forces between S. mutans (or S. gordonii) and C. albicans in the presen

45 unts (r = 0.412; p = 0.007), but not between S. mutans levels and either CD4+ counts or viral load.

46 was a bivariate linear relationship between S. mutans levels and CD8+ counts (r = 0.412; p = 0.007),

47 Given that the SRCR domains bind S. mutans and hydroxyapatite in the tooth, we investigat

48 mplexes with salivary constituents that bind S. mutans, thus representing a novel innate immune funct

49 Aortic specimens from both S. mutans and Sm+BA groups displayed increased numbers o

50 ented by rs12138897(G)) was characterized by S. mutans, Scardovia wiggsiae, Treponema sp. HOT268, Tan

51 ssion of the collagen-binding protein Cnm by S. mutans has been associated with extraoral infections,

52 an interfere with subsequent colonization by S. mutans in vitro.

53 bolism that restricts biofilm development by S. mutans.

54 ch detected up to 60% of proteins encoded by S. mutans within biofilms.

55 ion of oral keratinocytes and fibroblasts by S. mutans.

56 selectively inhibit the biofilm formation by S. mutans, indicative of its selectivity and non-bacteri

57 on of the pH-responsive atpB (PatpB::gfp) by S. mutans within microcolonies.

58 ently detected along with heavy infection by S. mutans in plaque biofilms from ECC-affected children.

59 Oral colonization of mice by S. mutans was impaired in the presence of anti-P1(39-512

60 esponsible for formation of microcolonies by S. mutans; these Gtf-mediated processes may enhance the

61 ately pH 6.0) but is gradually taken over by S. mutans as the latter species slowly starts decreasing

62 ssential for persistence and pathogenesis by S. mutans and provide evidence for a molecular connectio

63 ntly affect growth of or stress tolerance by S. mutans, whereas strains lacking pta were more sensiti

64 contributes to the pathogenicity of certain S. mutans strains in their native habitat, the oral cavi

65 In conclusion, S. mutans and S. sobrinus correlated with Romanian adole

66 In conclusion, S. mutans infection accelerated plaque growth, macrophag

67 Concomitantly, S. mutans became the major species in the mature biofilm

68 ively prevented dental caries by controlling S. mutans in a rat caries model without perturbing the o

69 lue is equally effective as MB in destroying S. mutans biofilms growing on plastic or collagen withou

70 3F1 dispersed S. mutans biofilms independently of biofilm-related fact

71 We report that S. parasanguinis disrupts S. mutans and C. albicans biofilm synergy in a contact a

72 pattern of CNV at DMBT1, and that the DMBT1-S. mutans interaction is a promising model of host-patho

73 A mutant library including each S. mutans TetR gene was constructed and the transcriptio

74 locked positive feedback circuits may enable S. mutans to fine-tune the kinetics and magnitude of the

75 vels detected (25-50 muM), farnesol enhanced S. mutans-biofilm cell growth, microcolony development,

76 The presence of C. albicans enhances S. mutans growth within biofilms, yet the chemical inter

77 es, S. agalactiae, S. dysgalactiae, S. equi, S. mutans, S. pneumoniae, S. suis and S. uberis, as well

78 notated 3F1 dispersed 50% of the established S. mutans biofilm but did not disperse biofilms formed b

79 extracellular glucans may selectively favor S. mutans binding interactions with C. albicans during c

80 Glucan production, which is critical for S. mutans biofilm formation, was also inhibited in 2-spe

81 at while Cnm is not universally required for S. mutans cariogenicity, it contributes to (i) the invas

82 Thus, Cnm is required for S. mutans invasion of endothelial cells and possibly rep

83 protein that modulates genes responsible for S. mutans-induced cariogenesis.

84 istinct protective and morphogenic roles for S. mutans, and these structures are functionally homolog

85 In growth conditions normally selective for S. mutans, Mg(2+) supplementation is able to increase th

86 ally that provide enhanced binding sites for S. mutans.

87 Our results suggest that, for S. mutans, mutator phenotypes, due to loss of BER enzyme

88 Consistent with this hypothesis, we found S. mutans strains defective in glucan production were mo

89 Of the four S. mutans serotypes (c, e, f, and k), serotype c strains

90 Furthermore, S. mutans up-regulates specific adaptation mechanisms to

91 gs provide insight into how the fast-growing S. mutans creates nutrient-depleted regions that affect

92 Here, S. mutans strains UA159 and GS-5 were examined for stoch

93 Our data provide insights about how S. mutans optimizes its metabolism and adapts/survives w

94 ntitative proteomics approach to examine how S. mutans produces relevant proteins that facilitate its

95 ur data provide mechanistic insight into how S. mutans regulates bimodality and explain the puzzle of

96 ce factors could provide new insights on how S. mutans may have become a major cariogenic pathogen.

97 However, S. mutans binding forces are dramatically enhanced when

98 Importantly, S. mutans has evolved a network of regulators to integra

99 In S. mutans, CSP is secreted as a 21-residue peptide; howe

100 suggesting the importance of this BL-BGC in S. mutans-mediated cariogenesity.

101 ort the clinical significance of a BL-BGC in S. mutans.

102 urpose of this study was to identify BGCs in S. mutans from a high-caries risk study population using

103 erized a diadenylate cyclase, named CdaA, in S. mutans.

104 rance, (p)ppGpp metabolism and competence in S. mutans.

105 ays for development of genetic competence in S. mutans.

106 entification of one such immunity complex in S. mutans strain GS-5 that confers protection against Sm

107 ersions of the peptides could be detected in S. mutans, and FLAG tagging of the peptides impaired the

108 No significant differences in S. mutans genotypes were found between the two groups ov

109 a FLAG epitope and shown to be expressed in S. mutans by Western blotting with an anti-FLAG antibody

110 ion factor regulating the frtP expression in S. mutans, thus affecting the intrinsic fluoride toleran

111 Via heterologous expression in S. mutans, we confirmed that GAS RmlB and RmlC are criti

112 only effective transporters of galactose in S. mutans.

113 d that in-frame deletion of the cdaA gene in S. mutans causes decreased c-di-AMP levels, increased se

114 induces the expression of virulence genes in S. mutans (e.g., gtfB, fabM).

115 the repertoire of oxidative stress genes in S. mutans, shedding new light on the role of Spx regulat

116 Inactivation of SMU.662, an LsrS homolog, in S. mutans strains UA159 and V403 rendered the cells refr

117 Furthermore, overexpression of LsrS in S. mutans created cells more susceptible to Smb.

118 llular DNA (eDNA) as a scaffolding matrix in S. mutans biofilms.

119 ttranslationally by a different mechanism in S. mutans and possibly in other streptococci.

120 r circuits controlling lactose metabolism in S. mutans, where LacR and CcpA integrate cellular and en

121 hat CdaA is an important global modulator in S. mutans and is required for optimal growth and environ

122 rough a CabPA/VicR/GtfB signaling network in S. mutans.

123 ways for sucrose utilization were present in S. mutans.

124 solutely necessary for mutacin production in S. mutans.

125 YlxM was observed as a produced protein in S. mutans.

126 test insights into global gene regulation in S. mutans, including mechanisms of signal transduction,

127 xplore the significance of Spx regulation in S. mutans.

128 , similar in appearance to those reported in S. mutans biofilm extracellular matrices, are reconstitu

129 ke hybrid (BL-BGC)-have not been reported in S. mutans.

130 Ultimately, this resulted in S. mutans dominance composition in the 3-species biofilm

131 circuit is the proximal regulator of sigX in S. mutans, and we infer that it controls competence in a

132 and energy generation against heat stress in S. mutans.

133 Thus, in S. mutans, serine-phosphorylated HPr functions in concer

134 er they are related to fluoride tolerance in S. mutans.

135 y sought to define a role for ylxM, which in S. mutans and numerous other bacteria resides directly u

136 erized by a panel of streptococci, including S. mutans, S. sobrinus, and Streptococcus australis, and

137 t is present in many streptococci, including S. mutans.

138 36) showed lower detection of taxa including S. mutans, changes not observed in children with follow-

139 Intriguingly, BF-CM induced S. mutans gtfBC expression (responsible for Gtf exoenzym

140 dicate that CA6 gene polymorphisms influence S. mutans colonization, tooth biofilm microbiota composi

141 minimal C-terminal region that could inhibit S. mutans adherence to SAG was also confirmed to be with

142 on of S. parasanguinis and nitrite inhibited S. mutans growth and biofilm formation in vitro.

143 t (SeLECT-Defense(TM) sealant) in inhibiting S. mutans and S. salivarius biofilm formation in vitro.

144 Moreover, S. parasanguinis inhibits S. mutans glucosyltransferase (GtfB) activity, which is

145 ver microparticles and antimicrobials inside S. mutans biofilms.

146 TF antimicrobial region (rs: 1126478) killed S. mutans in vitro.

147 A synthetic 11-mer LTF/K peptide killed S. mutans and other caries-related bacteria, while the L

148 The surface-localized S. mutans P1 adhesin contributes to tooth colonization a

149 from this cross-kingdom association modulate S. mutans build-up in biofilms.

150 glucose consumption of Streptococcus mutans (S. mutans) biofilms.

151 y, after demonstrating that ME kills >99% of S. mutans in planktonic cultures, 8 enamel slabs were ha

152 ts importance for the persistence ability of S. mutans in the oral cavity.

153 Our data show that the ability of S. mutans strains defective in the gtfB gene or the gtfB

154 The ability of S. mutans to respond to environmental stresses presented

155 ECC children in the presence and absence of S. mutans detection.

156 The enhanced binding affinity of S. mutans to glucan-coated C. albicans resulted in a lar

157 eria and viruses, and mediates attachment of S. mutans to hydroxyapatite on the surface of the tooth.

158 dding purified recombinant AtlA autolysin of S. mutans but was only partially restored by addition of

159 Biofilms of S. mutans, alone or mixed with Actinomyces naeslundii an

160 processes may enhance the competitiveness of S. mutans in the multispecies environment in biofilms on

161 quantify the rate of glucose consumption of S. mutans biofilms in the presence of sucrose.

162 und to completely inhibit the development of S. mutans and S. salivarius biofilms.

163 sumption profile in the local environment of S. mutans biofilm.

164 of microcolonies, and (iii) establishment of S. mutans in a multispecies biofilm in vitro using a nov

165 The virulence expression of S. mutans is linked to its stress adaptation to the chan

166 represents an important virulence factor of S. mutans that may contribute to cardiovascular infectio

167 equence diversity at the SAG-binding gene of S. mutans, and DMBT1 CNV.

168 and integrate a 73.7-kb BGC to the genome of S. mutans UA159 via three rounds of NabLC cloning.

169 The genotype of S. mutans was compared between 10 HIV-positive individua

170 BF-CM) significantly increased the growth of S. mutans and altered biofilm 3D-architecture in a dose-

171 ompound did not affect the overall growth of S. mutans and commensal oral bacteria, and selectively i

172 l genes, including nox, crucial to growth of S. mutans under conditions of oxidative stress.

173 2 was found to be critical for the growth of S. mutans under envelope stress conditions.

174 ) sealant completely inhibited the growth of S. mutans.

175 l accumulation in biofilms, the influence of S. mutans on fungal biology in this mixed-species relati

176 showed significantly increased inhibition of S. mutans adhesion to SAG, with less of an effect on SAG

177 A significant growth inhibition of S. mutans by direct contact illustrates successful encap

178 We concluded that killing of S. mutans by ME promotes effective remineralization of S

179 placed SeLECT-Defense sealant over a lawn of S. mutans.

180 The level of S. mutans colonization was determined by conventional cu

181 an have a significant effect on the level of S. mutans, but not genotypes.

182 s sp. HOT 071/070 (p = 0.023); and levels of S. mutans (p = 0.02) and Bifidobacteriaceae (p = 0.012)

183 ed a rapid pH drop in the microenviroment of S. mutans microcolonies prior to the decrease in the mac

184 patial pH changes in the microenvironment of S. mutans cells under both planktonic and biofilm condit

185 and characterized an ilvE deletion mutant of S. mutans UA159.

186 esis to screen for acid-sensitive mutants of S. mutans and identified an SMU.746-SMU.747 gene cluster

187 H with a more pronounced metabolic output of S. mutans.

188 The pathogenicity of S. mutans relies on the bacterium's ability to colonize

189 critical to persistence and pathogenicity of S. mutans.

190 networks in the biology and pathogenicity of S. mutans.

191 Persistence of S. mutans biofilms in the oral cavity can lead to tooth

192 hereby enhancing the pathogenic potential of S. mutans in advancing carious lesions.

193 The cariogenic potential of S. mutans is related to its ability to metabolize a wide

194 we aimed to investigate how the presence of S. mutans influences C. albicans biofilm development and

195 Surprisingly, the presence of S. mutans restored the biofilm-forming ability of C. alb

196 rmation, were upregulated in the presence of S. mutans.

197 nhanced biofilm formation in the presence of S. mutans.

198 38897) CCC associated with low prevalence of S. mutans (OR (95% CI): 0.5 (0.3, 0.8)), and caries (OR

199 ock 4 TTG associated with high prevalence of S. mutans (OR: 2.7 (1.2, 5.9)) and caries (OR: 2.3 (1.2,

200 The proportion of S. mutans decreased steadily in DMADDM-containing groups

201 by ME promotes effective remineralization of S. mutans-demineralized enamel compared with controls.

202 a statistically significant 99.9% removal of S. mutans biofilms exposed to the UAS for 10 s, relative

203 component of the acid-adaptive repertoire of S. mutans.

204 file the dynamic transcriptomic responses of S. mutans during physiological heat stress.

205 finding may explain the mutualistic role of S. mutans and C. albicans in cariogenic biofilms.

206 This study explored (i) the role of S. mutans Gtfs in the development of the EPS matrix and

207 , we present the complete genome sequence of S. mutans GS-5, a serotype c strain originally isolated

208 ated the potential for an invasive strain of S. mutans, OMZ175, to accelerate plaque growth in apolip

209 on the teeth, independent of diet, strain of S. mutans, simultaneous or sequential inoculation, or pr

210 ual-luciferase expressing reporter strain of S. mutans, we were able to exogenously control and measu

211 ide, was present in all sequenced strains of S. mutans but absent in all bacteria in current database

212 leria mellonella virulence model, strains of S. mutans deficient in Fpg, MutY and Smn showed increase

213 Surprisingly, mutant strains of S. mutans with impairment in RGP side chain modification

214 In vitro studies of S. mutans and Muc19 interactions (i.e. adherence, aggreg

215 ines and as a tool for functional studies of S. mutans P1.

216 Recent studies of S. mutans suggested that purified ComE binds to two 11-b

217 unctionally displayed on the cell surface of S. mutans as a fusion protein with SpaP.

218 for proper function of P1 on the surface of S. mutans.

219 udy demonstrates that selective targeting of S. mutans biofilms by 3F1 was able to effectively reduce

220 y interaction between the N and C termini of S. mutans P1 creates a non-adherent phenotype.

221 oduction/acid tolerance, and ATP turnover of S. mutans during heat stress.

222 or therapeutics to diminish the virulence of S. mutans.

223 Instead, the cell wall of S. mutans is highly decorated with rhamnose-glucose poly

224 ance delivery of antimicrobials into 3-d-old S. mutans biofilms.

225 Twelve-day-old S. mutans biofilms in the IP space were exposed to a pro

226 mulation is a late event, appearing in older S. mutans biofilms after 60 hours of growth.

227 nctionality-dependent proton accumulation on S. mutans surface.

228 hromosomal DNA alone had a limited effect on S. mutans adherence to saliva-coated hydroxylapatite bea

229 understand the impact of S. parasanguinis on S. mutans and C. albicans synergy.

230 Lactobacillus or S. mutans was found either at low levels or not present

231 The x-directional pH scan over S. mutans also showed the influence of the pH profile on

232 ress tolerance in the dental caries pathogen S. mutans.

233 n was lower among subjects with cnm-positive S. mutans expressing collagen binding activity.

234 for the presence or absence of cnm-positive S. mutans in the saliva by PCR and collagen binding acti

235 he collagen binding activity of cnm-positive S. mutans is related to the nature of the CMBs or to cog

236 Cnm-positive S. mutans was detected more often among subjects with CM

237 equired for functioning of the Gram-positive S. mutans YidC2 and was necessary to complement the E. c

238 nvironment produced by the lactate-producing S. mutans biofilm.

239 at the RGP has a distinct role in protecting S. mutans from a variety of stress conditions pertinent

240 Using purified S. mutans RpoD and Escherichia coli RNA polymerase, we a

241 ed and evaluated for their ability to reduce S. mutans biofilms, as well as inhibit the activity of G

242 nt of KK saliva with antibody to LTF reduced S. mutans killing in a dose-dependent manner (P = 0.02).

243 Caries induction reflected S. mutans or S. gordonii colonization abundance: the for

244 Mutation of lrgAB renders S. mutans more sensitive to oxidative, heat, and vancomy

245 Forty representative S. mutans isolates were selected for genome sequencing f

246 , as compared with animals that had a single S. mutans infection or were co-colonized with both bacte

247 esence of either diet, if inoculated singly, S. mutans always out-competed S. gordonii on the teeth,

248 ional biofilm architecture displays sizeable S. mutans microcolonies surrounded by fungal cells, whic

249 n and distribution by the cariogenic species S. mutans.

250 ess biofilm than the model cariogenic strain S. mutans UA159, suggesting the importance of this BL-BG

251 With sucrose, S. mutans produces exopolysaccharides to enhance bacteri

252 nticaries therapies that specifically target S. mutans biofilms but do not disturb the overall oral m

253 d a small molecule that specifically targets S. mutans biofilms.

254 layer interferometry (BLI) demonstrated that S. mutans YlxM interacts with the SRP components Ffh and

255 This study demonstrates that S. mutans produces eDNA by multiple avenues, including l

256 biofilm model of C. albicans, we found that S. mutans augmented haploid C. albicans accumulation in

257 Subsequently, we found that S. mutans-derived glucosyltransferase B (GtfB) itself ca

258 Results indicate that S. mutans ADP-Glc PPase is an allosteric regulatory enzy

259 Our results indicate that S. mutans within a mixed-species biofilm community incre

260 We observed that S. mutans levels were higher in HIV-infected individuals

261 Last, we report that S. mutans LiaS, a sensor kinase of the LiaFSR 3-componen

262 Further analyses revealed that S. mutans-derived exoenzyme glucosyltransferase B (GtfB)

263 Clinical studies have shown that S. mutans is often detected with Candida albicans in ear

264 e distinct patterns observed in the way that S. mutans responded to heat stress that included 66 tran

265 In contrast, GtfB bound uniformly across the S. mutans cell surface with less adhesion failure and a

266 anisms appears to be largely mediated by the S. mutans-derived exoenzyme glucosyltransferase B (GtfB)

267 ghts into a potential target to increase the S. mutans sensitivity to fluoride for a better preventio

268 ain O87 was successfully used to monitor the S. mutans acid production profiles within dual- and mult

269 The in-frame deletion of the S. mutans frtR gene resulted in decreased cell viability

270 s, we describe the functional domains of the S. mutans SloR protein and propose that the hyperactive

271 results identify YlxM as a component of the S. mutans SRP and suggest a regulatory function affectin

272 iofilms proved to be capable of reducing the S. mutans.

273 dy reinforces the importance of LrgAB to the S. mutans stress response.

274 aceae and Bifidobacteriaceae, in addition to S. mutans and S. wiggsiae, were associated with the pres

275 her, as compared with the enzyme adhesion to S. mutans.

276 and expression of comX and comY, compared to S. mutans UA159.

277 mixed or in MSN showed strong inhibition to S. mutans and L. casei.

278 within the comX gene that appears unique to S. mutans.

279 differentiates biofilms formed by wild-type S. mutans from a triple DeltaP1/WapA/Smu_63c mutant with

280 In the present study, using S. mutans strains with surface-displayed pH-sensitive pH

281 s accrue more biomass and harbor more viable S. mutans cells than single-species biofilms.

282 The major caries-associated species were S. mutans and S. wiggsiae, the latter of which is a cand

283 ene expression are in general augmented when S. mutans form mixed-species biofilms (vs. single-specie

284 these key virulence factors especially when S. mutans resides in multi-species microbial communities

285 rastic reduction in their abundance, whereas S. mutans' natural competitors, including health-associa

286 with limited access to dental care, whereas S. mutans and S. sobrinus were detected infrequently in

287 determine genotypic variants associated with S. mutans activity and reduced caries.

288 the regulation of processes associated with S. mutans pathogenesis.

289 When challenged with S. mutans and a cariogenic diet, total smooth and sulcal

290 pathways of C. albicans when cocultured with S. mutans in mixed biofilms.

291 higher (odds ratio = 14.3) in the group with S. mutans expressing collagen binding activity, as compa

292 f the BA and non-BA groups was infected with S. mutans (Sm).

293 ith S. parasanguinis prior to infection with S. mutans and received nitrite in the drinking water, as

294 ted with caries onset) when interacting with S. mutans, and a new cross-feeding mechanism mediated by

295 lic dependency or physical interactions with S. mutans suffered drastic reduction in their abundance,

296 une functions of saliva in interactions with S. mutans.

297 ognize the native protein and interfere with S. mutans adhesion in vitro.

298 but not from A. naeslundii, interfered with S. mutans BM71 colonization.

299 s colonization and to interact in vitro with S. mutans GtfB.

300 -uniform pH distribution was observed within S. mutans biofilms, reflecting differences in microbial