ライフサイエンスコーパス: T. denticola

1 T. denticola and its purified protease induced both MMP-

2 T. denticola Cpt catalyzed in vitro phosphatidylcholine

3 T. denticola Cpt complemented a Saccharomyces cerevisiae

4 T. denticola DNA was detected in the spleen, heart, and

5 T. denticola genomic DNA was detected in oral plaque sam

6 T. denticola grown in a serum-free medium did not exhibi

7 T. denticola induced significantly larger lesions in mic

8 T. denticola infection altered the expression of genes k

9 T. denticola is closely associated with periodontal dise

10 T. denticola parent and isogenic mutant strains, as well

11 T. denticola produces a number of virulence factors, inc

12 T. denticola tap1 and flanking DNA were identified, clon

13 T. denticola virulence, as evaluated by lesion size, was

14 T. denticola, along with Porphyromonas gingivalis and Ba

15 T. denticola-infected mice had higher levels of horizont

16 . gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola, 1.99 (0.992, 4.00), P = 0.052; T. forsythi

17 tion was investigated for P. gingivalis 381, T. denticola 35405, and mixtures of the two organisms us

18 Using published peptide sequences of a T. denticola surface-associated oligopeptidase with BANA

19 specificity, were not capable of resolving a T. denticola infection.

20 By utilizing a T. denticola gene inactivation system recently developed

21 MCP-1 levels were significantly lower after T. denticola challenge, and the kinetics suggested that

22 to be widely distributed and conserved among T. denticola isolates.

23 gingivalis in 15%, B. forsythus in 14%, and T. denticola in 18% of all subjects.

24 Elevated salivary MMP-8 and T. denticola biofilm levels displayed robust combinatori

25 2), P. gingivalis (OR = 1.12, 0.67-1.88) and T. denticola (OR = 1.34, 0.83-2.12) measured in plaque.

26 gingivalis, P. intermedia, T. forsythia, and T. denticola were more prevalent in CP; however, their m

27 omonas gingivalis, Tannerella forsythia, and T. denticola) in inducing disseminating infections in wi

28 (OR 4.17); P. gingivalis, B. forsythus, and T. denticola (OR 4.06); and P. gingivalis, P. nigrescens

29 nd B. forsythus (OR 3.84); P. gingivalis and T. denticola (OR 4.17); P. gingivalis, B. forsythus, and

30 ociated with EOP, and that P. gingivalis and T. denticola are of particular importance and may play a

31 e prevalence of Porphyromonas gingivalis and T. denticola associated significantly with ABL, whereas

32 3.23); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.59); with severe periodontitis (OR 4.

33 2.91); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.70) with the clinical diagnosis of sl

34 4.06); and P. gingivalis, P. nigrescens, and T. denticola (OR 3.29).

35 all other pts genes in both T. pallidum and T. denticola are actively expressed, the primary sensory

36 res were challenged with T. pectinovorum and T. denticola strains, and the supernatants were analyzed

37 cytoplasmic protein encoded in the annotated T. denticola genome.

38 subspecies pallidum monoclonal antibodies), T. denticola (serotypes A-D), T. socranskii subspecies b

39 Because T. denticola lacks lipopolysaccharides that serve as tar

40 An OR could not be calculated because T. denticola was not detected in health-associated plaqu

41 ituent proteins to allow interaction between T. denticola switch-basal body proteins and the flagella

42 lethal outcome following infection with both T. denticola and T. pectinovorum, suggesting an endotoxi

43 hat the primary function of FHL-1 binding by T. denticola might be to facilitate adherence to FHL-1 p

44 xis is involved in the tissue penetration by T. denticola.

45 is study, we investigated the role played by T. denticola periplasmic flagella (PF), unique motility

46 .02 to 7.03), but at lower risk for carrying T. denticola (OR, 0.42; 95% CI, 0.17 to 0.98).

47 ssociated Treponema spp. of the oral cavity (T. denticola and T. medium/T. vincentii) or genital area

48 ning the potential causative role of chronic T. denticola periodontal infection and vascular atherosc

49 ant Treponema denticola, an Escherichia coli-T. denticola shuttle vector that renders T. denticola re

50 The complete T. denticola flgE gene was cloned into the shuttle vecto

51 ae CPT1 mutant, and expression of the entire T. denticola LicCA-Cpt pathway in E. coli resulted in ph

52 ptide which enters the cytoplasm may explain T. denticola's relative resistance to human beta-defensi

53 d molecular patterns (PAMPs) responsible for T. denticola activation of the innate immune system are

54 protease, dentilisin, is not responsible for T. denticola insensitivity to defensins and examined sev

55 variety of thiol compounds as substrates for T. denticola to produce H(2)S.

56 Key pathogens P. gingivalis, T. forsythia, T. denticola, P. micra, C. rectus, and E. nodatum show s

57 significant for P. gingivalis, T. forsythia, T. denticola, P. micra, C. rectus, and E. nodatum.

58 used to purify a 52-kDa CGase activity from T. denticola, and high pressure liquid chromatography el

59 ntity with the partial sequence of CfpA from T. denticola, T. vincentii, and T. pallidum subsp. perte

60 Wild-type fliG genes from T. denticola and from Treponema pallidum were cloned int

61 of the putative switch basal body genes from T. denticola interfered with motility.

62 We have cloned the gene of GGT from T. denticola, which contains an open reading frame of 72

63 mogeneity four of the five PTS proteins from T. denticola.

64 The first family includes the sequence from T. denticola.

65 scending order of importance, P. gingivalis, T. denticola, and P. intermedia were the microorganisms

66 is study we hypothesized that P. gingivalis, T. denticola, and T. forsythia are synergistic in terms

67 most rats were infected with P. gingivalis, T. denticola, and T. forsythia as a consortium.

68 ApoE(-/-) mice infected with P. gingivalis, T. denticola, and T. forsythia as a polymicrobial infect

69 These results documented that P. gingivalis, T. denticola, and T. forsythia not only exist as a conso

70 ntal parameters and levels of P. gingivalis, T. denticola, and T. forsythia, but not A. actinomycetem

71 ats were infected with either P. gingivalis, T. denticola, or T. forsythia in monomicrobial infection

72 y the gene encoding trypsin-like activity in T. denticola and thus facilitate molecular-level studies

73 the PDD-associated Treponema isolates and in T. denticola, T. medium, and T. phagedenis.

74 Escherichia coli reporter constructs and in T. denticola.

75 tanding the contribution of FHL-1 binding in T. denticola pathogenesis and in development of periodon

76 as severely reduced, indicating that CheA in T. denticola mainly controls cellular reversal and that

77 The prcB gene is conserved in T. denticola strains.

78 Allelic replacement mutagenesis of cpt in T. denticola resulted in abrogation of phosphatidylcholi

79 The licCA gene was disrupted in T. denticola by erythromycin cassette mutagenesis, resul

80 reponemal proteases is not a major factor in T. denticola resistance.

81 id enables high-level expression of genes in T. denticola and possesses an efficient selectable marke

82 To reveal the role of c-di-GMP in T. denticola, a TDE0214 deletion mutant (TdDelta214) was

83 rrA gene, but the gene was not identified in T. denticola ATCC 33520.

84 Moreover, the enzymatic activity(ies) in T. denticola responsible for glutathione breakdown was i

85 mbly of outer membrane complexes involved in T. denticola interaction with host cells and tissue.

86 In order to analyze the functions of LrrA in T. denticola, an lrrA-inactivated mutant of strain ATCC

87 ggest that the dmcB gene codes for an MCP in T. denticola which may interact with other MCPs in these

88 ubsequently was performed to localize Msp in T. denticola.

89 d protein kinase (MAPK) signaling pathway in T. denticola-stimulated monocytes identified a prolonged

90 osphatidylcholine is a major phospholipid in T. denticola, accounting for 35-40% of total phospholipi

91 ate of production of another phospholipid in T. denticola, phosphatidylethanolamine, was elevated con

92 us T. pallidum flaA gene from the plasmid in T. denticola.

93 Nonpolar deletion of prcB in T. denticola showed that PrcB is required for production

94 y among aminopeptidase activities present in T. denticola and the proposed location of the enzyme in

95 eptides in other bacteria, and their role in T. denticola's relative resistance to beta-defensins was

96 ate that ERK1/2 and p38 play a major role in T. denticola-mediated pro- and anti-inflammatory cytokin

97 A mutation caused a reduction of swarming in T. denticola ATCC 35405 and consequently attenuated tiss

98 Indeed, T. denticola has been shown to have an iron-regulated 44

99 minal amino acid sequence analysis indicated T. denticola PFs are composed of one class A sheath prot

100 Immunofluorescence analysis of intact T. denticola revealed that only MOSP(C) contains surface

101 The plasmid was electroporated into T. denticola, and double-crossover recombinants which ha

102 An isogenic T. denticola opdB mutant was constructed by allelic repl

103 crease was statistically significant for log T. denticola counts.

104 s revealed that the TDE0143 deletion mutant (T. denticola DeltatbpA) had a decreased ability to trans

105 P. gingivalis 381, but not T. denticola strains, formed biofilms in vitro.

106 In this study we investigated the ability of T. denticola to bind the complement regulatory proteins

107 to the rC-Msp fragment, blocked adhesion of T. denticola ATCC 35405 cells to a range of host protein

108 ability to modify the virulence capacity of T. denticola and T. pectinovorum by environmental condit

109 ibe the purification and characterization of T. denticola CGase.

110 The two known chemoreceptors of T. denticola, DmcA and DmcB, also appear to be involved

111 at the unusual outer membrane composition of T. denticola may discourage cationic peptide binding.

112 for comparative purposes, one strain each of T. denticola, T. medium, T. vincentii, and T. phagedenis

113 useful in studying the virulence factors of T. denticola and uncultivatible pathogenic spirochetes.

114 n modifies the flagellin proteins (FlaBs) of T. denticola by O-linkage at multiple sites near the D1

115 ciated with the extracytoplasmic fraction of T. denticola and expresses multifunctional properties.

116 In vitro growth of T. denticola and T. pectinovorum as a function of modifi

117 In contrast, growth of T. denticola or T. pectinovorum under iron-limiting cond

118 be used in future studies of interactions of T. denticola with host cells and tissue.

119 otease inhibitors did not enhance killing of T. denticola by h beta D-2, suggesting that degradation

120 ene was cloned from genomic DNA libraries of T. denticola.

121 le in the flagellar assembly and motility of T. denticola.

122 e major sheath (or surface) protein (Msp) of T. denticola is implicated in adhesion of bacteria to ho

123 he construction of a specific flgE mutant of T. denticola ATCC 35405 following electroporation utiliz

124 er, by using dentilisin-deficient mutants of T. denticola, we found that T. denticola preferentially

125 network in the biology and pathogenicity of T. denticola.

126 hese findings indicated that the presence of T. denticola and unidentified spirochetes in health-asso

127 he GGT may play a role in the propagation of T. denticola within inflamed periodontal tissues.

128 against the major outer membrane protein of T. denticola GM-1 and ATCC 35405 did not cross-react wit

129 d sequences of the FlaA and FlaB proteins of T. denticola were most similar to those of T. pallidum a

130 echanisms responsible for the recognition of T. denticola by the innate immune system and the underly

131 esults indicated that different serotypes of T. denticola had similar abilities to attach to epitheli

132 the ability of FHL-1 bound to the surface of T. denticola to serve as a cofactor for factor I-mediate

133 ylhydrazone, increased the susceptibility of T. denticola to killing by hbetaD-3, demonstrating a pot

134 ive two-component regulatory system (TCS) of T. denticola that is formed by the products of open read

135 may play important roles in the virulence of T. denticola.

136 impact that TDE0214 has on the virulence of T. denticola.

137 cassette (ABC) efflux pumps had no effect on T. denticola's susceptibility to hbetaD-2 or -3.

138 tudies confirm a causal link for active oral T. denticola infection with both atheroma and periodonta

139 periodontal disease induced by chronic oral T. denticola infection and atherosclerosis in hyperlipid

140 estingly, unlike the T. pallidum orthologue, T. denticola TroR (TroR(Td)) possesses a C-terminal Src

141 In the human pathogen T. denticola, purine biosynthesis should depend on avail

142 stimulate, and the complemented PF-positive T. denticola strain restored the activation.

143 ation with the two other previously purified T. denticola enzymes, gamma-glutamyltransferase and cyst

144 oli-T. denticola shuttle vector that renders T. denticola resistant to coumermycin was constructed.

145 escent in situ hybridization (FISH) revealed T. denticola clusters in both gingival and aortic tissue

146 e immunoreactive products has revealed seven T. denticola genes which appear to encode homologs of fl

147 demonstrated that hbpA is present in several T. denticola ATCC strains and clinical isolates, but not

148 lutathione metabolism in the oral spirochete T. denticola; our results suggest that glutathione metab

149 . mutans, S. sanguis, Selenomonas sputigena, T. denticola, and T. vincentii) were present.

150 Thus it appears that T. denticola does contain a licCA-dependent CDP-choline

151 In this study, we demonstrate that T. denticola induces innate immune responses via the uti

152 We demonstrate that T. denticola PurE (TdPurE) is AIR carboxylase, the first

153 Here we demonstrate that T. denticola specifically binds FHL-1 via a 14-kDa, surf

154 Southern blot analysis demonstrated that T. denticola ATCC 35405 expresses the lrrA gene, but the

155 Nonetheless, we demonstrated that T. denticola binds significantly less hbetaD-2 and -3 th

156 ent methods, we previously demonstrated that T. denticola proteases are not responsible for decreased

157 cient mutants of T. denticola, we found that T. denticola preferentially binds FH and not FHL-1, and

158 The results indicate that T. denticola has high pathogenicity, including dissemina

159 Previous studies have indicated that T. denticola stimulates the innate immune system through

160 ensin (h beta D) binding, we postulated that T. denticola would resist killing by h beta D.

161 These results prove that T. denticola contains the entire three-step pathway to p

162 TLR2/1 and TLR2/6 heterodimers revealed that T. denticola predominantly utilizes TLR2/6 for the induc

163 advances our understanding of the role that T. denticola plays in the development and progression of

164 Here, we show that T. denticola FlgE self-catalyses an interpeptide crossli

165 Our findings show that T. denticola possesses a unique phosphatidylcholine synt

166 We showed that T. denticola is resistant to h beta D-1 and -2.

167 These findings suggest that T. denticola stimulates the innate immune system in a TL

168 The T. denticola enzyme can be regarded as a true PIPase, si

169 The T. denticola genome is considerably larger in size than

170 The T. denticola isolates demonstrated significant trypsin-l

171 train 381 rgpB and fimA genes as well as the T. denticola flgE and cfpA genes.

172 Cleavage of FH by the T. denticola protease, dentilisin, may contribute to the

173 Bound FH is rapidly cleaved by the T. denticola protease, dentilisin.

174 opeptidases, the preferred substrate for the T. denticola protein is Cys-Gly (k cat/Km of 8.2 microm(

175 equence of a predicted 52-kDa protein in the T. denticola genome data base.

176 Cou, and the vector was transformed into the T. denticola ATCC 33520 flgE erythromycin-resistant knoc

177 rporated the interrupted tap1 genes into the T. denticola chromosome, creating Tap1-deficient mutants

178 Functional domains of the T. denticola CheA and CheY proteins are highly conserved

179 In this report, the structure of the T. denticola FH-binding protein, FhbB, was solved to 1.7

180 Analysis of the T. denticola genome reveals factors mediating coaggregat

181 dB, in an apparently noncoding region of the T. denticola genome unannotated contigs.

182 d in localization and oligomerization of the T. denticola major surface protein (Msp).

183 ne the cellular location and topology of the T. denticola polypeptide.

184 whereas freeze-fracture EM revealed that the T. denticola outer membrane contains heterogeneous trans

185 ts suggest a specific mechanism by which the T. denticola protease may disrupt homeostatic processes

186 ld belief that Msp forms an array within the T. denticola outer membrane and demonstrate, instead, th

187 whether Msp forms an array on or within the T. denticola outer membrane.

188 Thus, T. denticola has two novel hemin binding proteins which

189 Importantly, GNA, when added to T. denticola, was able to compete with glutathione and i

190 a-FhbB Ab can compete with FH for binding to T. denticola and block dentilisin-mediated FH cleavage.

191 s that regulate the inflammatory response to T. denticola are currently unresolved.

192 Wild-type T. denticola and the purified PF triggered activation of

193 Wild-type T. denticola ATCC 35405 was found to penetrate the tissu

194 Wild-type T. denticola stimulated the production of the cytokines

195 cytopathic to host cells, and FhbB, a unique T. denticola lipoprotein that binds complement regulator

196 While T. denticola also induced IL-6 and IL-8 production, thes

197 m to induce a robust MCP-1 production, while T. denticola appeared to inhibit this activity of the fi

198 givalis 381 formed synergistic biofilms with T. denticola 35405.

199 med synergistic biofilms when incubated with T. denticola strains.

200 -/-) mice (n = 24) were orally infected with T. denticola ATCC 35404 and were euthanized after 12 and

201 was observed in SCID mice mono-infected with T. denticola, whereas abscesses were rare in SCID mice i

202 Primary infection with T. denticola induced a significant (400-fold) serum immu

203 ct of mono-infection of the dental pulp with T. denticola and with polymicrobial "red-complex" organi

204 of the isolates showed cross-reactivity with T. denticola.