ライフサイエンスコーパス: S. mutans

1 S. mutans cells subjected to mechanical extraction were

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

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

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

5 S. mutans may also be associated with atherosclerotic pl

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

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

8 S. mutans recoveries were significantly reduced both in

9 S. mutans SRP pathway mutants demonstrate growth defects

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

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

12 S. mutans was often observed at high levels in the early

13 S. mutans-positive children had higher food cariogenicit

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

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

16 In addition, S. mutans BM71 colonized more efficiently on the sgc pro

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

18 de (H(2)O(2)) to compete effectively against S. mutans.

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

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

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

22 rmation) demonstrate Muc19 poorly aggregates S. mutans.

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

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

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

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

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

28 Food frequency, putative cariogenicity, and S. mutans were associated with S-ECC individually and in

29 (p < 0.0001) were associated with S-ECC, and S. mutans with S. sobrinus was associated with lesion re

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

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

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

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

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

35 llus fermentum, Lactobacillus vaginalis, and S. mutans with Streptococcus sobrinus (all p < 0.05) wer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 agglutinin inhibited biofilm development by S. mutans in the absence of sucrose, and whole saliva wa

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

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

53 onstituents to moderate biofilm formation by S. mutans through P1-dependent and P1-independent pathwa

54 We have examined biofilm formation by S. mutans UA159, and derivative strains carrying mutatio

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

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

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

58 ies lesion scores for the rats inoculated by S. mutans and fed the DSMZ16671 supplement, by compariso

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 of the S-ECC S. mutans strains but not in CF S. mutans strains.

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

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

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

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

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

71 diet; un-inoculated/16671-supplemented diet; S. mutans 10449S-inoculated/placebo diet; and un-inocula

72 3F1 dispersed S. mutans biofilms independently of biofilm-related fact

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

74 iomarkers) present in 88 to 95% of the S-ECC S. mutans strains but not in CF S. mutans strains.

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

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

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

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

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

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

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

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

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

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

85 of specific-pathogen-free rats were formed: S. mutans 10449S-inoculated/16671-supplemented diet; un-

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

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

88 dy was to identify common DNA fragments from S. mutans present in S-ECC but not in CF children.

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

90 Because most humans harbor S. mutans, but not all manifest disease, it has been pro

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

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

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

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

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

96 o function as a transcriptional activator in S. mutans.

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

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

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

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

101 tors that regulate the expression of covR in S. mutans UA159.

102 competence and the proper control of DDAG in S. mutans.

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

104 ative regulator of competence development in S. mutans.

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

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

107 sion and induction of cel gene expression in S. mutans.

108 ed in the upregulation of clpP expression in S. mutans.

109 ific for the induction of clpP expression in S. mutans.

110 tigated the regulation of clpP expression in S. mutans.

111 only effective transporters of galactose in S. mutans.

112 sensor kinases in the expression of gbpC in S. mutans strain UA159.

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

121 existence of a global regulatory network in S. mutans that governs the utilization of non-preferred

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 ot clear how covR expression is regulated in S. mutans.

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

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

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

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

131 tion of gene expression but revealed that in S. mutans there is a substantial CcpA-independent networ

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

133 s involved in superoxide stress tolerance in S. mutans.

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

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

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

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

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

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

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

141 ver microparticles and antimicrobials inside S. mutans biofilms.

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

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

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

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

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

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

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

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

150 ted that loss of CcpA impacts the ability of S. mutans to transport and grow on selected sugars.

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

152 d salivary agglutinin-induced aggregation of S. mutans was adversely affected by the loss of P1 and s

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

154 It mediates attachment of S. mutans to tooth surfaces and has been a focus for imm

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

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

157 d can contribute toward the cariogenicity of S. mutans.

158 CiaR and CiaH of S. mutans comprise a two-component signal transduction s

159 nterfere with the subsequent colonization of S. mutans BM71 on the existing streptococcal biofilms.

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

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

162 enes for the fructose/mannose-EII enzymes of S. mutans (manL, fruI and levD) enhances levD expression

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

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

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

166 ystal structure of the A(3)VP(1) fragment of S. mutans AgI/II that demonstrates a unique fibrillar fo

167 Using the fructan hydrolase (fruA) gene of S. mutans as a model, we demonstrated that CcpA plays a

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

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 ) sealant completely inhibited the growth of S. mutans.

174 His-AbpB caused a 1.4- to 2-fold increase of S. mutans Gtf-B sucrase activity and a 3- to 6-fold incr

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 expression of the bacteriocin mutacin IV of S. mutans, as well as the H(2)O(2)-dependent release of

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

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

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

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

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

184 streptococci and the survival mechanisms of S. mutans in the oral biofilm.

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

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

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

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

189 e, methyl viologen (MV)-sensitive mutants of S. mutans were generated via ISS1 mutagenesis.

190 In an animal study, the average number of S. mutans colonies recovered from the teeth of rats infe

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

192 sible functional role in the pathogenesis of S. mutans associated with dental caries.

193 better understanding of the pathogenesis of S. mutans, as well as providing further insight into the

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

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

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

197 IPS is important for the persistence of S. mutans grown in batch culture with excess glucose and

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

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

200 rectly modulates the pathogenic potential of S. mutans through global control of gene expression.

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

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

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

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

205 for CodY in two key virulence properties of S. mutans.

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

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

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

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

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

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

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

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

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

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

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

217 se, it has been proposed that the strains of S. mutans associated with S-ECC are genetically distinct

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

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

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

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

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

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

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

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

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

227 in the expression of key virulence traits of S. mutans and indicates that the underlying mechanisms b

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

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

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

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

232 eractions, the effect of S. gordonii AbpB on S. mutans Gtf-B activity was also tested.

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

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

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

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

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

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

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

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

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

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

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

244 Providing S. mutans with synthetic fragments of ComS revealed that

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

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

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

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

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

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

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

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

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

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

255 We hypothesized: (1) that S. mutans recoveries from rats' teeth in vivo will decre

256 We demonstrated that S. mutans BM71 colonized much less efficiently in vitro

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

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

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

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

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

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

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

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

265 volved in BCAA biosynthesis, suggesting that S. mutans CodY is not activated by GTP.

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

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

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

269 dii, produced proteases that inactivated the S. mutans CSP.

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

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

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

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

274 Searching the S. mutans genome, we identified two putative spx genes,

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

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

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

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

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

280 ding of a beneficial immumomodulatory mAb to S. mutans increased exposure of that epitope.

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

282 enes were expressed differently in wild-type S. mutans when glucose- and galactose-grown cells were c

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

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

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

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

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

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

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

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

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

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

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

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

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