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1 in the flagellar assembly and motility of T. denticola.
2 (previously T. forsythensis), and Treponema denticola.
3 cherichia coli reporter constructs and in T. denticola.
4 the isolates showed cross-reactivity with T. denticola.
5 eneity four of the five PTS proteins from T. denticola.
6 were Fusobacterium nucleatum and Prevotella denticola.
7 play important roles in the virulence of T. denticola.
8 e first family includes the sequence from T. denticola.
9 was cloned from genomic DNA libraries of T. denticola.
10 is involved in the tissue penetration by T. denticola.
11 rmedia, Prevotella nigrescens, and Treponema denticola.
12 equently was performed to localize Msp in T. denticola.
13 ogy to the major sheath protein of Treponema denticola.
14 T. pallidum flaA gene from the plasmid in T. denticola.
15 twork in the biology and pathogenicity of T. denticola.
16 pact that TDE0214 has on the virulence of T. denticola.
17 , P. intermedia, T. forsythia, and Treponema denticola.
18 givalis, Tannerella forsythia, and Treponema denticola.
19 rom the pathogenic oral spirochete Treponema denticola.
20 onas micra, Filifactor alocis, and Treponema denticola.
22 ingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola, 1.99 (0.992, 4.00), P = 0.052; T. forsythia,
23 n was investigated for P. gingivalis 381, T. denticola 35405, and mixtures of the two organisms using
25 ), Tannerella forsythia (98%/84%), Treponema denticola (94%/74%), Parvimonas micra (86%/62%), Campylo
26 d structure in the oral spirochete Treponema denticola, a keystone pathogen of periodontitis was repo
27 entified and include the anaerobe Prevotella denticola, a Lysobacter sp., and members of the Ricketts
35 hatidylcholine is a major phospholipid in T. denticola, accounting for 35-40% of total phospholipid.
36 ngivalis, Tannerella forsythensis, Treponema denticola, Actinobacillus actinomycetemcomitans) and den
37 olecular patterns (PAMPs) responsible for T. denticola activation of the innate immune system are cur
40 ontaneous coumermycin A1-resistant Treponema denticola, an Escherichia coli-T. denticola shuttle vect
42 order to analyze the functions of LrrA in T. denticola, an lrrA-inactivated mutant of strain ATCC 354
43 nidase (TDE0471) was identified in Treponema denticola, an oral spirochaete associated with human per
44 hbB Ab can compete with FH for binding to T. denticola and block dentilisin-mediated FH cleavage.
50 enables high-level expression of genes in T. denticola and possesses an efficient selectable marker t
51 e genetic regulatory mechanisms of Treponema denticola and present an overview of the possible roles
53 ciated Treponema spp. of the oral cavity (T. denticola and T. medium/T. vincentii) or genital area (T
55 hal outcome following infection with both T. denticola and T. pectinovorum, suggesting an endotoxin-l
56 h protein (MOSP(N) and MOSP(C)) of Treponema denticola and that TprC(C) is solely responsible for bet
58 he gene encoding trypsin-like activity in T. denticola and thus facilitate molecular-level studies of
62 eful in studying the virulence factors of T. denticola and uncultivatible pathogenic spirochetes.
63 of mono-infection of the dental pulp with T. denticola and with polymicrobial "red-complex" organisms
64 includes Porphyromonas gingivalis, Treponema denticola, and "Tannerella forsythia" (opinion on name c
65 forsythia, Prevotella intermedia, Treponema denticola, and Aggregatibacter actinomycetemcomitans was
66 the MotB proteins of T. pallidum, Treponema denticola, and Borrelia burgdorferi have membrane topolo
67 ncluding Porphyromonas gingivalis, Treponema denticola, and Campylobacter rectus, were highest in pat
71 ed to purify a 52-kDa CGase activity from T. denticola, and high pressure liquid chromatography elect
72 gingivalis, Tannerella forsythia, Treponema denticola, and Prevotella intermedia was evaluated quali
73 gingivalis, Tannerella forsythia, Treponema denticola, and Streptococcus oralis were measured with r
74 study we hypothesized that P. gingivalis, T. denticola, and T. forsythia are synergistic in terms of
76 oE(-/-) mice infected with P. gingivalis, T. denticola, and T. forsythia as a polymicrobial infection
77 se results documented that P. gingivalis, T. denticola, and T. forsythia not only exist as a consorti
78 l parameters and levels of P. gingivalis, T. denticola, and T. forsythia, but not A. actinomycetemcom
79 found in Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythensis, to determine the
80 ation of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia and some evidence su
84 sting of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, as an oral lavage e
85 omitans, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, as well as Actinomy
86 vels of Gram-negative bacteria and Treponema denticola, and the prevalence of Porphyromonas gingivali
87 o induce a robust MCP-1 production, while T. denticola appeared to inhibit this activity of the fibro
88 l other pts genes in both T. pallidum and T. denticola are actively expressed, the primary sensory tr
90 Both Porphyromonas gingivalis and Treponema denticola are frequently associated together in these or
91 l Treponema species, in particular Treponema denticola, are associated with the progression of human
92 , periodontal pathogens, including Treponema denticola, are believed to initiate the destructive infl
94 a primary virulence determinant in Treponema denticola, as well as the parental ortholog for the Trep
95 presence of the periodontopathogen Treponema denticola, as well as with the clinical parameters of pe
96 revalence of Porphyromonas gingivalis and T. denticola associated significantly with ABL, whereas oth
97 , and the vector was transformed into the T. denticola ATCC 33520 flgE erythromycin-resistant knockou
99 ) mice (n = 24) were orally infected with T. denticola ATCC 35404 and were euthanized after 12 and 24
100 utation caused a reduction of swarming in T. denticola ATCC 35405 and consequently attenuated tissue
101 the rC-Msp fragment, blocked adhesion of T. denticola ATCC 35405 cells to a range of host protein mo
102 Southern blot analysis demonstrated that T. denticola ATCC 35405 expresses the lrrA gene, but the ge
103 tream from the previously isolated Treponema denticola ATCC 35405 prtB gene coding for a chymotrypsin
106 onstrated that hbpA is present in several T. denticola ATCC strains and clinical isolates, but not in
107 te 2,843,201-bp genome sequence of Treponema denticola (ATCC 35405) an oral spirochete associated wit
108 rmedia, Prevotella nigrescens, and Treponema denticola before and following mechanical periodontal th
112 ase inhibitors did not enhance killing of T. denticola by h beta D-2, suggesting that degradation of
113 odifies the flagellin proteins (FlaBs) of T. denticola by O-linkage at multiple sites near the D1 dom
114 anisms responsible for the recognition of T. denticola by the innate immune system and the underlying
116 P-1 levels were significantly lower after T. denticola challenge, and the kinetics suggested that thi
119 rated the interrupted tap1 genes into the T. denticola chromosome, creating Tap1-deficient mutants.
121 ent in situ hybridization (FISH) revealed T. denticola clusters in both gingival and aortic tissue of
126 evealed that the TDE0143 deletion mutant (T. denticola DeltatbpA) had a decreased ability to transpor
132 on with the two other previously purified T. denticola enzymes, gamma-glutamyltransferase and cystaly
139 ics of humoral immune responses to Treponema denticola following primary infection, reinfection, and
141 cter species, Eikenella corrodens, Treponema denticola, Gemella haemolysans, Granulicatella adiacens,
151 Based on these results, we propose that T.denticola has evolved a strategy to scavenge host sialic
154 ivalis, Bacteroides forsythus, and Treponema denticola in 150 children and adolescents, 4 to 16 years
158 nas gingivalis, Tannerella forsythia, and T. denticola) in inducing disseminating infections in wild-
162 riodontal disease induced by chronic oral T. denticola infection and atherosclerosis in hyperlipidemi
163 ies confirm a causal link for active oral T. denticola infection with both atheroma and periodontal d
165 tease, dentilisin, is not responsible for T. denticola insensitivity to defensins and examined severa
173 ajor sheath (or surface) protein (Msp) of T. denticola is implicated in adhesion of bacteria to host
174 nd a gold drug, auranofin, against Treponema denticola is mediated through inhibition of the metaboli
177 The spirochete dental pathogen Treponema denticola lacks a purK gene and contains a class II purE
179 CPT1 mutant, and expression of the entire T. denticola LicCA-Cpt pathway in E. coli resulted in phosp
180 e), and group 3 (Treponema putidum/Treponema denticola-like) were present in 96.1%, 98%, and 76.5% of
181 opathic to host cells, and FhbB, a unique T. denticola lipoprotein that binds complement regulatory p
182 severely reduced, indicating that CheA in T. denticola mainly controls cellular reversal and that act
183 genome encodes 12 orthologs of the Treponema denticola major sheath protein (Msp) prompted us to reex
186 that ERK1/2 and p38 play a major role in T. denticola-mediated pro- and anti-inflammatory cytokine p
187 the primary function of FHL-1 binding by T. denticola might be to facilitate adherence to FHL-1 pres
189 h antibodies (above the median) to Treponema denticola (odds ratio [OR]=1.7; 95% CI, 1.2 to 2.3), Pre
192 3); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.59); with severe periodontitis (OR 4.65)
193 1); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.70) with the clinical diagnosis of sligh
195 R 4.17); P. gingivalis, B. forsythus, and T. denticola (OR 4.06); and P. gingivalis, P. nigrescens, a
196 B. forsythus (OR 3.84); P. gingivalis and T. denticola (OR 4.17); P. gingivalis, B. forsythus, and T.
197 P. gingivalis (OR = 1.12, 0.67-1.88) and T. denticola (OR = 1.34, 0.83-2.12) measured in plaque.
199 were infected with either P. gingivalis, T. denticola, or T. forsythia in monomicrobial infections o
200 athione metabolism in the oral spirochete T. denticola; our results suggest that glutathione metaboli
201 belief that Msp forms an array within the T. denticola outer membrane and demonstrate, instead, that
202 reas freeze-fracture EM revealed that the T. denticola outer membrane contains heterogeneous transmem
204 hete, contains 12 orthologs of the Treponema denticola outer membrane major sheath protein has engend
207 ey pathogens P. gingivalis, T. forsythia, T. denticola, P. micra, C. rectus, and E. nodatum show stat
210 ding the contribution of FHL-1 binding in T. denticola pathogenesis and in development of periodontal
211 g the potential causative role of chronic T. denticola periodontal infection and vascular atheroscler
212 study, we investigated the role played by T. denticola periplasmic flagella (PF), unique motility org
213 of production of another phospholipid in T. denticola, phosphatidylethanolamine, was elevated consid
214 vances our understanding of the role that T. denticola plays in the development and progression of pe
219 2/1 and TLR2/6 heterodimers revealed that T. denticola predominantly utilizes TLR2/6 for the inductio
220 nt mutants of T. denticola, we found that T. denticola preferentially binds FH and not FHL-1, and tha
223 thione by the periodontal pathogen Treponema denticola produces hydrogen sulfide, which may play a ro
224 suggest a specific mechanism by which the T. denticola protease may disrupt homeostatic processes req
227 methods, we previously demonstrated that T. denticola proteases are not responsible for decreased vu
228 ptidases, the preferred substrate for the T. denticola protein is Cys-Gly (k cat/Km of 8.2 microm(-1)
229 uch as Porphyromonas gingivalis or Treponema denticola) provided highly accurate predictions of perio
232 ia (formally T. forsythensis), and Treponema denticola relative to 40 oral bacteria at each test site
234 -T. denticola shuttle vector that renders T. denticola resistant to coumermycin was constructed.
235 Moreover, the enzymatic activity(ies) in T. denticola responsible for glutathione breakdown was inac
236 Allelic replacement mutagenesis of cpt in T. denticola resulted in abrogation of phosphatidylcholine
237 Immunofluorescence analysis of intact T. denticola revealed that only MOSP(C) contains surface-ex
238 ides in other bacteria, and their role in T. denticola's relative resistance to beta-defensins was in
239 de which enters the cytoplasm may explain T. denticola's relative resistance to human beta-defensins.
242 truction of a new Escherichia coli-Treponema denticola shuttle vector based on the naturally occurrin
243 Treponema denticola, an Escherichia coli-T. denticola shuttle vector that renders T. denticola resis
244 a, Prevotella intermedia (Pi), and Treponema denticola significantly more in group A than group B.
247 rotein kinase (MAPK) signaling pathway in T. denticola-stimulated monocytes identified a prolonged up
249 Previous studies have indicated that T. denticola stimulates the innate immune system through To
251 were challenged with T. pectinovorum and T. denticola strains, and the supernatants were analyzed fo
255 gingivalis, Tannerella forsythia, Treponema denticola, Streptococcus oralis, and Actinomyces naeslun
257 Using published peptide sequences of a T. denticola surface-associated oligopeptidase with BANA-hy
260 comparative purposes, one strain each of T. denticola, T. medium, T. vincentii, and T. phagedenis.
261 ty with the partial sequence of CfpA from T. denticola, T. vincentii, and T. pallidum subsp. pertenue
262 mitans), Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia (previously T. forsythen
263 omitans, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Actinomyces naeslun
265 rtium of Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucle
267 he nucleotide (nt) sequence of the Treponema denticola (Td) DNA gyrase beta-subunit gene (gyrB) has b
269 g), Tannerella forsythia (Tf), and Treponema denticola (Td) was performed using real-time polymerase
270 A chemotaxis gene cluster from Treponema denticola (Td), a pathogenic spirochete associated with
271 s (Pg), Tannerella forsythia (Tf), Treponema denticola (Td), and Dialister pneumosintes were determin
272 (Pg), Prevotella intermedia (Pi), Treponema denticola (Td), and Escherichia coli using reverse trans
273 the air-sensitive oral spirochete, Treponema denticola (Td), is a principal enzymatic scavenger of su
274 onstituent of the cell envelope of Treponema denticola (TDE) and one of its principal virulence deter
275 the trans-enoyl-CoA reductase from Treponema denticola (tdTer), which has been utilized for the engin
276 two-component regulatory system (TCS) of T. denticola that is formed by the products of open reading
278 this study we investigated the ability of T. denticola to bind the complement regulatory proteins fac
279 m human serum proteins; it is required for T.denticola to grow in a medium that mimics gingival crevi
280 ydrazone, increased the susceptibility of T. denticola to killing by hbetaD-3, demonstrating a potent
282 ability of FHL-1 bound to the surface of T. denticola to serve as a cofactor for factor I-mediated c
283 ed with Treponema pectinovorum and Treponema denticola to test three specific hypotheses: (i) these t
284 ed to detect Treponema amylovorum, Treponema denticola, Treponema maltophilum, Treponema medium, Trep
285 ingly, unlike the T. pallidum orthologue, T. denticola TroR (TroR(Td)) possesses a C-terminal Src hom
286 disease-associated oral spirochete Treponema denticola using an oral epithelial cell line-based exper
288 rodens, Bacteroides forsythus, and Treponema denticola was investigated in 25 smokers and 25 non-smok
289 em to generate specific mutants in Treponema denticola was utilized to determine if Tap1 was essentia
291 by using dentilisin-deficient mutants of T. denticola, we found that T. denticola preferentially bin
293 ivalis, Bacteroides forsythus, and Treponema denticola were identified from multiple subjects, but ty
294 givalis, P. intermedia, T. forsythia, and T. denticola were more prevalent in CP; however, their mere
295 ix months after SRP, the counts of Treponema denticola were significantly reduced in both groups (bot
296 observed in SCID mice mono-infected with T. denticola, whereas abscesses were rare in SCID mice infe
297 st that the dmcB gene codes for an MCP in T. denticola which may interact with other MCPs in these or
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