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1                                              F. nucleatum activated p38 and c-Jun NH(2)-terminal kina
2                                              F. nucleatum activates IL-1beta processing through the N
3                                              F. nucleatum also promoted invasion of KB cells by other
4                                              F. nucleatum and C. rectus were also associated with EOP
5                                              F. nucleatum and S. cristatus coaggregate strongly via a
6                                              F. nucleatum binding to clinical adenocarcinomas correla
7                                              F. nucleatum biofilm coculture with OD-E model causes la
8                                              F. nucleatum cell wall and FAD-I induced hBD2 via TLR2.
9                                              F. nucleatum isolated from other parts of the body may o
10                                              F. nucleatum ssp. nucleatum and ssp. polymorphum signifi
11                                              F. nucleatum strains isolated from amniotic fluids and p
12                                              F. nucleatum treatment induced apoptosis of PBMCs and PM
13                                              F. nucleatum was first detected in the blood vessels in
14                                              F. nucleatum was systematically detected in samples with
15 tabase further correctly identified 28 of 34 F. nucleatum clinical isolates to the subspecies level.
16 either Actinobacillus actinomycetemcomitans, F. nucleatum, or P. gingivalis.
17                                 In addition, F. nucleatum seems to be important for the development o
18 he IL-8 secreted from epithelial cells after F. nucleatum stimulation could be down-regulated by subs
19                                          All F. nucleatum strains stimulated significant increase in
20 trophils were significantly increased in all F. nucleatum groups compared with control (P <0.001).
21                                     Although F. nucleatum vincentii also reduced superoxide generatio
22                                     Although F. nucleatum vincentii also reduced superoxide generatio
23 mcomitans exhibited mutualism, and, although F. nucleatum was unable to grow with either of the other
24                 It is highly conserved among F. nucleatum, Fusobacterium periodonticum, and Fusobacte
25 tial role for this enzyme in establishing an F. nucleatum intracellular niche.
26 ort the isolation and characterization of an F. nucleatum (ATCC 25586)-associated defensin inducer (F
27  we present the first characterization of an F. nucleatum Type Vd phospholipase class A1 autotranspor
28 colonization of A. actinomycetemcomitans and F. nucleatum/periodonticum was not statistically associa
29 P. gingivalis, A. actinomycetemcomitans, and F. nucleatum was found to be higher in healthy individua
30 physical interaction between C. albicans and F. nucleatum and for the first time revealed the identit
31 that the interaction between C. albicans and F. nucleatum leads to a mutual attenuation of virulence,
32 physical interaction between C. albicans and F. nucleatum was mediated by the carbohydrate components
33  the regulation of hBD-2 mRNA; TNF-alpha and F. nucleatum cell wall induced hBD-2 mRNA rapidly (2 to
34 etected in the matching AF, with E. coli and F. nucleatum as the most prevalent.
35 capable of transforming Escherichia coli and F. nucleatum ATCC 10953 was constructed with pFN1.
36 ccharides isolated from Escherichia coli and F. nucleatum were poor stimulants of hBD-2, although the
37                          In both E. coli and F. nucleatum, FadA exists in two forms, the intact pre-F
38 stainings were negative in both controls and F. nucleatum cocultures.
39  A. actinomycetemcomitans, E. corrodens, and F. nucleatum was determined using an immunoassay.
40  sequential challenge with P. gingivalis and F. nucleatum and vice versa were approximately identical
41 periodontitis induced by a P. gingivalis and F. nucleatum mixed infection, and also on the local host
42     Infection of mice with P. gingivalis and F. nucleatum strains elicited lesions of various sizes a
43 hages that were exposed to P. gingivalis and F. nucleatum, without impairing their viability.
44  with/without priming with P. gingivalis and F. nucleatum.
45  and F. nucleatum but not with S. oralis and F. nucleatum, indicating that P. gingivalis and S. orali
46                 The aggregation of PBMCs and F. nucleatum T18 was inhibited by either L-arginine, L-l
47       Also, it grew with Veillonella sp. and F. nucleatum but not with S. oralis and F. nucleatum, in
48 ygen requirements (E. coli, A. viscosus, and F. nucleatum), as well as a model mammalian cell line (m
49              We suggest that A. aphrophilus, F. nucleatum, and S. intermedius are key pathogens for t
50     These miRNAs can enter bacteria, such as F. nucleatum and E. coli, specifically regulate bacteria
51                                           At F. nucleatum/P. gingivalis ratios of > or = 1:1, spreadi
52  Coaggregation-mediated interactions between F. nucleatum and other species facilitated the survival
53                    The CoAg reaction between F. nucleatum and the Candida species involved a heat-lab
54                   The CoAg reactions between F. nucleatum and the Candida species may be important in
55      Moreover, anti-FAD-I antibodies blocked F. nucleatum induction of hBD-2 by more than 80%.
56 l cavity, and the CoAg of C. dubliniensis by F. nucleatum when grown at 37 degrees C provides a rapid
57 iological pathways significantly impacted by F. nucleatum and S. gordonii included the mitogen-activa
58                  However, hBD-2 induction by F. nucleatum was not blocked by pretreatment with two NF
59 NK partially blocked hBD-2 mRNA induction by F. nucleatum, and the combination of two inhibitors comp
60 hat T cell activities were also inhibited by F. nucleatum via Fap2.
61 BD-2 induction, and that hBD-2 regulation by F. nucleatum is via p38 and JNK, while phorbol ester ind
62 ls of CCL20 at 6 h, following stimulation by F. nucleatum cell wall (FnCW).
63 helial cell, as well as protein synthesis by F. nucleatum.
64 her bacteria linked to colorectal carcinoma, F. nucleatum does not exacerbate colitis, enteritis, or
65                 Interestingly, in flow cells F. nucleatum and A. actinomycetemcomitans exhibited mutu
66   In this study, a fadA-complementing clone, F. nucleatum 12230 USF81, was constructed.
67                                 By contrast, F. nucleatum strains contain genomic expansions of Type
68                                 In contrast, F. nucleatum was able to coaggregate not only with both
69 igher levels of P. intermedia, E. corrodens, F. nucleatum, and IL-1beta than non-users.
70 is designed to determine impact of different F. nucleatum strains on neutrophil function.
71 culture in the presence/absence of different F. nucleatum strains.
72              The invasive ability may enable F. nucleatum to colonize and infect the pregnant uterus.
73                     In the oral environment, F. nucleatum adheres to a large diversity of species, fa
74                Given its prevalence in EONS, F. nucleatum should be placed on the same importance sca
75                         In addition to FadA, F. nucleatum ATCC 25586 and ATCC 49256 also encode two p
76                 MALDI-TOF MS spectra of five F. nucleatum subspecies (animalis, fusiforme, nucleatum,
77 dentical and were lower than those following F. nucleatum challenge alone and higher than control lev
78 eficient mice (C57BL/6 TLR2(-/-)), following F. nucleatum infection.
79  11% for Porphyromonas gingivalis to 40% for F. nucleatum.
80  may be an important virulence mechanism for F. nucleatum to infect the placenta.
81  endothelial receptor for FadA, required for F. nucleatum binding to the cells.
82 resent the first complementation studies for F. nucleatum.
83 lecular analyses demonstrated that cell-free F. nucleatum membranes are sufficient to induce cell dea
84 ious studies identified a novel adhesin from F. nucleatum, FadA, as being involved in the attachment
85 those of native FAD-I (nFAD-I) isolated from F. nucleatum ATCC 25586.
86  select subtype(s) of a given species, e.g., F. nucleatum subspecies animalis and polymorphum and S.
87                  Although a trend for higher F. nucleatum and P. gingivalis concentrations in aCCP-po
88 r caspase-3 was expressed in controls and in F. nucleatum laboratory strain ATCC cocultures throughou
89 rginine-inhibitable adhesin-encoding gene in F. nucleatum that is involved in interspecies coadherenc
90  The role of TNF-alpha as an intermediary in F. nucleatum signaling was ruled out by addition of anti
91 routing into the connective tissue matrix in F. nucleatum OD-E cocultures.
92  of the outer membrane family of proteins in F. nucleatum.
93        Thus, FadA plays an important role in F. nucleatum colonization in vivo.
94 o studies to determine its potential role in F. nucleatum pathogenesis.
95 ence of a restriction-modification system in F. nucleatum.
96  the cells attached to the tooth, whereas in F. nucleatum biofilm-treated cultures, the Ki-67-express
97 t this hypothesis, we intravenously injected F. nucleatum into pregnant CF-1 mice.
98         Additionally, intravenously injected F. nucleatum localizes to mouse tumor tissues in a Fap2-
99 ent of S. cristatus to adherent and invading F. nucleatum.
100 tum was augmented compared with that of live F. nucleatum.
101                             Mechanistically, F. nucleatum targeted TLR4 and MYD88 innate immune signa
102 emcomitans, A. viscosus, B. melaninogenicus, F. nucleatum, P. gingivalis, P. intermedia, S. mutans, S
103                     The fadA deletion mutant F. nucleatum 12230 US1 was defective in host cell attach
104     A double-crossover fadA deletion mutant, F. nucleatum 12230-US1, was constructed by utilizing a n
105          Effects of Fusobacterium nucleatum (F. nucleatum) biofilm on epithelial cell proliferation,
106 n (Anaerobe Helsinki Negative [AHN] 9508) of F. nucleatum was placed on the top of the model.
107                               The ability of F. nucleatum 12230, US1, and USF81 to colonize the mouse
108                               The ability of F. nucleatum to induce apoptosis was abolished by either
109                               The ability of F. nucleatum to inhibit mononuclear cell proliferation m
110    The effects of the presence or absence of F. nucleatum on anaerobe survival in both the biofilm an
111   In an equivalent culture in the absence of F. nucleatum, the numbers of black-pigmented anaerobes (
112 nsible for arginine-inhibitable adherence of F. nucleatum and provides definitive molecular evidence
113 attachment loss >2 mm, whereas the amount of F. nucleatum DNA did.
114  epidemiological evidence for association of F. nucleatum and P. aeruginosa with OSCC.
115 eractions were involved in the attachment of F. nucleatum to KB cells.
116 ractions are also involved in the binding of F. nucleatum to host cells.
117                The metabolic capabilities of F. nucleatum revealed by its genome are therefore consis
118  were aggregated in the presence of cells of F. nucleatum but not control bacteria.
119 e attachment and invasion characteristics of F. nucleatum were also tested using KB cells, an oral ep
120 present study, we showed that coinfection of F. nucleatum and T. forsythia is more potent than infect
121  were isolated from the membrane fraction of F. nucleatum ATCC 23726 and identified via mass spectros
122                             Co-incubation of F. nucleatum and Escherichia coli enhanced penetration o
123                                Inhibition of F. nucleatum host cell attachment and invasion with gala
124                A spontaneous mutant, lam, of F. nucleatum, isolated as defective in autoagglutination
125                             A DNA library of F. nucleatum FDC 364 was constructed by partial digestio
126                           Using a library of F. nucleatum mutants, we found that the Fap2 protein of
127                       Possible mechanisms of F. nucleatum's role in the pathogenesis of periodontal d
128 t was significantly lower than the number of F. nucleatum-positive subjects around teeth (P < 0.05).
129                                The number of F. nucleatum-positive subjects around the implant was si
130 ERT-2 epithelial cells with equal numbers of F. nucleatum and S. cristatus bacteria led to significan
131 albicans SN152 mutant library and a panel of F. nucleatum 23726 outer membrane protein mutants, we id
132 ortant for understanding the pathogenesis of F. nucleatum.
133         Although the phagocytosis pattern of F. nucleatum in the mixed infection remained similar to
134                   Neutrophil phagocytosis of F. nucleatum ssp. polymorphum was significantly greater
135                   Neutrophil phagocytosis of F. nucleatum ssp. polymorphum was significantly greater
136                   Neutrophil phagocytosis of F. nucleatum strains and neutrophil apoptosis were analy
137  cells may reflect the invasive phenotype of F. nucleatum and contribute to the greater pathogenic po
138 ibute to the greater pathogenic potential of F. nucleatum than of S. gordonii.
139                           In the presence of F. nucleatum, anaerobes persisted in high numbers (>10(7
140 m mutants, we found that the Fap2 protein of F. nucleatum directly interacted with TIGIT, leading to
141  in which tumors exploit the Fap2 protein of F. nucleatum to inhibit immune cell activity via TIGIT.
142 tokines and CCL20 suggests the broad role of F. nucleatum and human antimicrobial peptides in primary
143 uld improve our understanding of the role of F. nucleatum in periodontal infections.
144  indicate that the immunosuppressive role of F. nucleatum is largely due to the ability of this organ
145 lated bone resorption and that the strain of F. nucleatum used appeared to be the strongest inducer o
146 e findings suggest that different strains of F. nucleatum impact neutrophil function in different way
147                               All strains of F. nucleatum significantly increased phagocytic capacity
148  with human and cynomolgus monkey strains of F. nucleatum.
149 l induction of hBD-2 by different strains of F. nucleatum; ATCC 25586 and ATCC 23726 induce significa
150 rphum was significantly greater than that of F. nucleatum ssp. polymorphum significantly blocked fMLP
151 rphum was significantly greater than that of F. nucleatum ssp. vincentii and ssp. nucleatum (P <0.001
152  species involved a heat-labile component on F. nucleatum and a mannan-containing heat-stable recepto
153 ached P. gingivalis but had no influences on F. nucleatum bacterial adherence.
154 valis simultaneously (at different sites) or F. nucleatum administered within 4 h prior to or 1 h fol
155                                     Overall, F. nucleatum and S. gordonii perturbed the gingival epit
156 he presence of any orange-complex pathogens (F. nucleatum, P. intermedia, and C. rectus), total cance
157 A may be a therapeutic target for preventing F. nucleatum colonization of the host.
158 ains, indicating that FAD-I is the principal F. nucleatum agent for hBD-2 induction in HOECs.
159                                 The purified F. nucleatum immunosuppressive protein (FIP) is composed
160 ore, the yeast form of C. albicans repressed F. nucleatum-induced MCP-1 and TNFalpha production in ma
161                     Hemagglutination of some F. nucleatum strains is also galactose sensitive, sugges
162                                  Strikingly, F. nucleatum achieves virulence in the absence of large,
163                               In this study, F. nucleatum was shown to activate both TLR2 and TLR4 in
164 e latter in the transwell assays, suggesting F. nucleatum may serve as an 'enabler' for other microor
165 ther of the other species in the peg system, F. nucleatum stimulated the growth of Veillonella sp. an
166                      Measuring and targeting F. nucleatum and its associated pathway will yield valua
167                              Thus, targeting F. nucleatum Fap2 or host epithelial Gal-GalNAc may redu
168               Recently, we demonstrated that F. nucleatum ATCC 23726 coaggregates with C. albicans SN
169 erleukin-6 (IL-6) and IL-8 demonstrated that F. nucleatum induced production of these cytokines, wher
170 tic and functional studies demonstrated that F. nucleatum promoted colorectal cancer resistance to ch
171 udies provided an initial demonstration that F. nucleatum adhered to and invaded HGEC and that this w
172  provides definitive molecular evidence that F. nucleatum adhesins play a vital role in inter-species
173 his study represents the first evidence that F. nucleatum may be transmitted hematogenously to the pl
174                                We found that F. nucleatum ATCC 23726 inhibits growth and hyphal morph
175                  These studies indicate that F. nucleatum aggregates PBMCs, and that this interaction
176                           Data indicate that F. nucleatum impaired endothelial cell proliferation and
177                  These studies indicate that F. nucleatum may facilitate the colonization of epitheli
178                 The data also indicated that F. nucleatum-induced cell apoptosis requires activation
179 tic analysis of sequence data indicates that F. nucleatum, F. necrophorum, and F. varium are the spec
180                We have shown previously that F. nucleatum adheres to and invades host epithelial and
181         However, inhibitor studies show that F. nucleatum stimulation of hBD-2 mRNA requires both new
182                         These data show that F. nucleatum subspecies and T. forsythia synergistically
183                Previously, it was shown that F. nucleatum induced preterm and term stillbirth in mice
184             Previous studies have shown that F. nucleatum species synergize with T. forsythia during
185                                          The F. nucleatum strain ATCC 25586 genome was assembled from
186           pHS17 was stably maintained in the F. nucleatum transformants, and differences in the trans
187 ine macrophage cell line, we showed that the F. nucleatum-induced inhibition of Candida hyphal morpho
188 erminal sequences of these proteins with the F. nucleatum genome revealed that the genes encoding the
189                   Our data support that this F. nucleatum-mediated inhibition is mediated by human, b
190                                        Thus, F. nucleatum orchestrates a molecular network of the Tol
191 0018), to P. gingivalis (P = 0.0013), and to F. nucleatum (P = 0.0200) than women who delivered at te
192        In addition, polyclonal antibodies to F. nucleatum, which inhibited fusobacterial attachment t
193       Tumors from Apc(Min/+) mice exposed to F. nucleatum exhibit a proinflammatory expression signat
194 lecular level, the genetically transformable F. nucleatum strain ATCC 23726 was screened for adherenc
195 t the strong coaggregation between wild-type F. nucleatum 23726 and C. albicans SN152 in an in vitro
196 mors is inhibited in the presence of various F. nucleatum strains.
197                                         When F. nucleatum T18 was incubated with PHA-stimulated PBMCs
198 r the 6-month period in both groups, whereas F. nucleatum was significantly reduced in all visits in
199                         This may explain why F. nucleatum is often found in mixed infections.
200 d C. albicans strains demonstrated CoAg with F. nucleatum.
201 ns grown at 37 degrees C to coaggregate with F. nucleatum.
202 ly C. dubliniensis strains coaggregated with F. nucleatum ATCC 49256 and no C. albicans strains showe
203 truction either alone or in combination with F. nucleatum.
204 were strong TLR4 agonists when combined with F. nucleatum LPS.
205 into neutrophil-like cells and cultured with F. nucleatum strains of subspecies (ssp.) nucleatum ATCC
206 incentii (FNV), and compare that genome with F. nucleatum ATCC 25586 (FN).
207                               Infection with F. nucleatum and P. gingivalis simultaneously (at differ
208                       Primary infection with F. nucleatum plus P. gingivalis at various ratios (i.e.,
209 an gingival epithelial cells stimulated with F. nucleatum cell wall extract, indicating possible invo
210 by immunofluorescence in HGE stimulated with F. nucleatum cell wall, consistent with induction of the
211 helium, in contrast to cultures treated with F. nucleatum clinical strain AHN, in which caspase-3 was
212 the polymicrobial consortium with or without F. nucleatum exhibited significantly increased alveolar

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