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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 induces the mobilization of immune cel
4                                              F. nucleatum also promoted invasion of KB cells by other
5                                              F. nucleatum and C. rectus were also associated with EOP
6                                              F. nucleatum and S. cristatus coaggregate strongly via a
7                                              F. nucleatum binding to clinical adenocarcinomas correla
8                                              F. nucleatum biofilm coculture with OD-E model causes la
9                                              F. nucleatum cell wall and FAD-I induced hBD2 via TLR2.
10                                              F. nucleatum isolated from other parts of the body may o
11                                              F. nucleatum ssp nucleatum, ssp polymorphum and P. gingi
12                                              F. nucleatum ssp polymorphum caused considerable mortali
13                                              F. nucleatum ssp. nucleatum and ssp. polymorphum signifi
14                                              F. nucleatum strains isolated from amniotic fluids and p
15                                              F. nucleatum synthesizes lanthionine for its peptidoglyc
16                                              F. nucleatum treatment induced apoptosis of PBMCs and PM
17                                              F. nucleatum was first detected in the blood vessels in
18                                              F. nucleatum was systematically detected in samples with
19 tabase further correctly identified 28 of 34 F. nucleatum clinical isolates to the subspecies level.
20 either Actinobacillus actinomycetemcomitans, F. nucleatum, or P. gingivalis.
21                                 In addition, F. nucleatum seems to be important for the development o
22 he IL-8 secreted from epithelial cells after F. nucleatum stimulation could be down-regulated by subs
23                                          All F. nucleatum strains stimulated significant increase in
24 trophils were significantly increased in all F. nucleatum groups compared with control (P <0.001).
25                                     Although F. nucleatum lacks canonical RNA chaperones, such as Hfq
26                                     Although F. nucleatum vincentii also reduced superoxide generatio
27                                     Although F. nucleatum vincentii also reduced superoxide generatio
28 mcomitans exhibited mutualism, and, although F. nucleatum was unable to grow with either of the other
29                 It is highly conserved among F. nucleatum, Fusobacterium periodonticum, and Fusobacte
30 tial role for this enzyme in establishing an F. nucleatum intracellular niche.
31 ort the isolation and characterization of an F. nucleatum (ATCC 25586)-associated defensin inducer (F
32  we present the first characterization of an F. nucleatum Type Vd phospholipase class A1 autotranspor
33 colonization of A. actinomycetemcomitans and F. nucleatum/periodonticum was not statistically associa
34 P. gingivalis, A. actinomycetemcomitans, and F. nucleatum was found to be higher in healthy individua
35 rs, Gardnerella vaginalis, S. agalactiae and F. nucleatum to vaginal epithelial cells is partially me
36 physical interaction between C. albicans and F. nucleatum and for the first time revealed the identit
37 that the interaction between C. albicans and F. nucleatum leads to a mutual attenuation of virulence,
38 physical interaction between C. albicans and F. nucleatum was mediated by the carbohydrate components
39  the regulation of hBD-2 mRNA; TNF-alpha and F. nucleatum cell wall induced hBD-2 mRNA rapidly (2 to
40  to the Bayesian bivariate LCM, S. bovis and F. nucleatum had a more significant predictive accuracy
41 iate LCMs, the sensitivities of S. bovis and F. nucleatum were calculated as 93% (95% CrI 0.84-0.98)
42 rated that the sensitivities of S. bovis and F. nucleatum were estimated to be 86% [95% credible inte
43     Bacterial species including S. bovis and F. nucleatum were measured by absolute quantitative real
44 CrI 0.73-0.85) respectively for S. bovis and F. nucleatum.
45 etected in the matching AF, with E. coli and F. nucleatum as the most prevalent.
46 capable of transforming Escherichia coli and F. nucleatum ATCC 10953 was constructed with pFN1.
47 ccharides isolated from Escherichia coli and F. nucleatum were poor stimulants of hBD-2, although the
48                          In both E. coli and F. nucleatum, FadA exists in two forms, the intact pre-F
49 stainings were negative in both controls and F. nucleatum cocultures.
50  A. actinomycetemcomitans, E. corrodens, and F. nucleatum was determined using an immunoassay.
51  sequential challenge with P. gingivalis and F. nucleatum and vice versa were approximately identical
52 otential, and consortia of P. gingivalis and F. nucleatum are synergistically pathogenic within in vi
53 periodontitis induced by a P. gingivalis and F. nucleatum mixed infection, and also on the local host
54     Infection of mice with P. gingivalis and F. nucleatum strains elicited lesions of various sizes a
55        Increased levels of P. gingivalis and F. nucleatum were associated with periodontitis in both
56 -10 after incubations with P. gingivalis and F. nucleatum, as well as significantly reduced the expre
57 hages that were exposed to P. gingivalis and F. nucleatum, without impairing their viability.
58  with/without priming with P. gingivalis and F. nucleatum.
59    S. mutans, S. sanguis, P. gingivalis, and F. nucleatum were incubated with serial dilutions (1/4,
60  and F. nucleatum but not with S. oralis and F. nucleatum, indicating that P. gingivalis and S. orali
61                 The aggregation of PBMCs and F. nucleatum T18 was inhibited by either L-arginine, L-l
62 for example, Fusobacterium periodonticum and F. nucleatum) and donor abundance.
63       Also, it grew with Veillonella sp. and F. nucleatum but not with S. oralis and F. nucleatum, in
64 ygen requirements (E. coli, A. viscosus, and F. nucleatum), as well as a model mammalian cell line (m
65 -P. gingivalis, anti-P. intermedia, and anti-F. nucleatum antibody concentrations displayed significa
66 001 and p = 0.020, respectively), while anti-F. nucleatum was positively associated with IgG anti-MAA
67              We suggest that A. aphrophilus, F. nucleatum, and S. intermedius are key pathogens for t
68     These miRNAs can enter bacteria, such as F. nucleatum and E. coli, specifically regulate bacteria
69                                           At F. nucleatum/P. gingivalis ratios of > or = 1:1, spreadi
70  Coaggregation-mediated interactions between F. nucleatum and other species facilitated the survival
71 tants, we investigated the interplay between F. nucleatum outer membrane protein RadD and different S
72                    The CoAg reaction between F. nucleatum and the Candida species involved a heat-lab
73                   The CoAg reactions between F. nucleatum and the Candida species may be important in
74      Moreover, anti-FAD-I antibodies blocked F. nucleatum induction of hBD-2 by more than 80%.
75 l cavity, and the CoAg of C. dubliniensis by F. nucleatum when grown at 37 degrees C provides a rapid
76 utral and sialic acid-terminating glycans by F. nucleatum.
77 iological pathways significantly impacted by F. nucleatum and S. gordonii included the mitogen-activa
78 f HDAC1 recapitulated the effects induced by F. nucleatum or butyrate.
79 he expression of interferon-gamma induced by F. nucleatum.
80                  However, hBD-2 induction by F. nucleatum was not blocked by pretreatment with two NF
81 NK partially blocked hBD-2 mRNA induction by F. nucleatum, and the combination of two inhibitors comp
82 hat T cell activities were also inhibited by F. nucleatum via Fap2.
83 BD-2 induction, and that hBD-2 regulation by F. nucleatum is via p38 and JNK, while phorbol ester ind
84 ls of CCL20 at 6 h, following stimulation by F. nucleatum cell wall (FnCW).
85 MCPIP-1 protein expression was suppressed by F. nucleatum and MALT-1 protein expression was suppresse
86  MALT-1 protein expression was suppressed by F. nucleatum, P. gingivalis LPS and IL-1beta.
87 helial cell, as well as protein synthesis by F. nucleatum.
88 her bacteria linked to colorectal carcinoma, F. nucleatum does not exacerbate colitis, enteritis, or
89                 Interestingly, in flow cells F. nucleatum and A. actinomycetemcomitans exhibited mutu
90 a-, or IL-10-producing cells after challenge F. nucleatum.
91   In this study, a fadA-complementing clone, F. nucleatum 12230 USF81, was constructed.
92                                 By contrast, F. nucleatum strains contain genomic expansions of Type
93                                 In contrast, F. nucleatum was able to coaggregate not only with both
94                            While controlling F. nucleatum through antibiotics could reduce cancer sev
95 igher levels of P. intermedia, E. corrodens, F. nucleatum, and IL-1beta than non-users.
96 is designed to determine impact of different F. nucleatum strains on neutrophil function.
97 culture in the presence/absence of different F. nucleatum strains.
98              The invasive ability may enable F. nucleatum to colonize and infect the pregnant uterus.
99 accessible because of the lack of endogenous F. nucleatum sialidase.
100                     In the oral environment, F. nucleatum adheres to a large diversity of species, fa
101                Given its prevalence in EONS, F. nucleatum should be placed on the same importance sca
102 ological research has now firmly established F. nucleatum as an oncomicrobe associated with several m
103                         In addition to FadA, F. nucleatum ATCC 25586 and ATCC 49256 also encode two p
104                 MALDI-TOF MS spectra of five F. nucleatum subspecies (animalis, fusiforme, nucleatum,
105 dentical and were lower than those following F. nucleatum challenge alone and higher than control lev
106 eficient mice (C57BL/6 TLR2(-/-)), following F. nucleatum infection.
107  11% for Porphyromonas gingivalis to 40% for F. nucleatum.
108  may be an important virulence mechanism for F. nucleatum to infect the placenta.
109  endothelial receptor for FadA, required for F. nucleatum binding to the cells.
110 resent the first complementation studies for F. nucleatum.
111  developing diagnostics and therapeutics for F. nucleatum.
112 lecular analyses demonstrated that cell-free F. nucleatum membranes are sufficient to induce cell dea
113 ious studies identified a novel adhesin from F. nucleatum, FadA, as being involved in the attachment
114 those of native FAD-I (nFAD-I) isolated from F. nucleatum ATCC 25586.
115                      Conditioned medium from F. nucleatum-infected HCT116 cells caused naive cells to
116  select subtype(s) of a given species, e.g., F. nucleatum subspecies animalis and polymorphum and S.
117                                  gingivalis, F. nucleatum, S. sanguis, and A. naeslundii were grown o
118 mRNA levels were increased by P. gingivalis, F. nucleatum, and IL-1beta, however, no changes were obs
119                  Although a trend for higher F. nucleatum and P. gingivalis concentrations in aCCP-po
120                               We discuss how F. nucleatum potentially uses this lactate utilization g
121 r caspase-3 was expressed in controls and in F. nucleatum laboratory strain ATCC cocultures throughou
122 rginine-inhibitable adhesin-encoding gene in F. nucleatum that is involved in interspecies coadherenc
123                          Knockout of hisR in F. nucleatum results in a small but reproducible lag in
124  The role of TNF-alpha as an intermediary in F. nucleatum signaling was ruled out by addition of anti
125 routing into the connective tissue matrix in F. nucleatum OD-E cocultures.
126  of the outer membrane family of proteins in F. nucleatum.
127 ns, little is known about gene regulation in F. nucleatum itself, including global stress-response pa
128 racterization of a global stress response in F. nucleatum, the genetic tools developed here will enab
129        Thus, FadA plays an important role in F. nucleatum colonization in vivo.
130 o studies to determine its potential role in F. nucleatum pathogenesis.
131 ence of a restriction-modification system in F. nucleatum.
132  the cells attached to the tooth, whereas in F. nucleatum biofilm-treated cultures, the Ki-67-express
133 ular migration were attenuated by inhibiting F. nucleatum host-cell binding and entry using galactose
134 t this hypothesis, we intravenously injected F. nucleatum into pregnant CF-1 mice.
135         Additionally, intravenously injected F. nucleatum localizes to mouse tumor tissues in a Fap2-
136 no-mupirocin was active against intratumoral F. nucleatum, a tumor promoting bacteria that accumulate
137 ent of S. cristatus to adherent and invading F. nucleatum.
138 heroid microenvironment, whereas heat-killed F. nucleatum is internalized and sequestered in the canc
139 tum was augmented compared with that of live F. nucleatum.
140 ed, in part due to challenges in maintaining F. nucleatum viability under standard aerobic cell cultu
141                             Mechanistically, F. nucleatum targeted TLR4 and MYD88 innate immune signa
142 emcomitans, A. viscosus, B. melaninogenicus, F. nucleatum, P. gingivalis, P. intermedia, S. mutans, S
143                     The fadA deletion mutant F. nucleatum 12230 US1 was defective in host cell attach
144 lidase-producing vaginal microbiotas, mutant F. nucleatum unable to consume sialic acids was impaired
145     A double-crossover fadA deletion mutant, F. nucleatum 12230-US1, was constructed by utilizing a n
146     The presence of Fusobacterium nucleatum (F. nucleatum) and Bacteroides fragilis (B. fragilis) in
147 erformance of fecal Fusobacterium nucleatum (F. nucleatum) and Streptococcus bovis (S. bovis) for tim
148          Effects of Fusobacterium nucleatum (F. nucleatum) biofilm on epithelial cell proliferation,
149 n (Anaerobe Helsinki Negative [AHN] 9508) of F. nucleatum was placed on the top of the model.
150                               The ability of F. nucleatum 12230, US1, and USF81 to colonize the mouse
151                               The ability of F. nucleatum to induce apoptosis was abolished by either
152                               The ability of F. nucleatum to inhibit mononuclear cell proliferation m
153    The effects of the presence or absence of F. nucleatum on anaerobe survival in both the biofilm an
154   In an equivalent culture in the absence of F. nucleatum, the numbers of black-pigmented anaerobes (
155 nsible for arginine-inhibitable adherence of F. nucleatum and provides definitive molecular evidence
156 scriptional level, and the administration of F. nucleatum or butyrate enhanced NVDR by increasing DAT
157 attachment loss >2 mm, whereas the amount of F. nucleatum DNA did.
158  epidemiological evidence for association of F. nucleatum and P. aeruginosa with OSCC.
159 eractions were involved in the attachment of F. nucleatum to KB cells.
160 ractions are also involved in the binding of F. nucleatum to host cells.
161                The metabolic capabilities of F. nucleatum revealed by its genome are therefore consis
162  were aggregated in the presence of cells of F. nucleatum but not control bacteria.
163 e attachment and invasion characteristics of F. nucleatum were also tested using KB cells, an oral ep
164 present study, we showed that coinfection of F. nucleatum and T. forsythia is more potent than infect
165 ural space infection may be a combination of F. nucleatum group and/or S. intermedius, with or withou
166 a provide further evidence on the effects of F. nucleatum on endothelium adhesion molecule abundance
167  were isolated from the membrane fraction of F. nucleatum ATCC 23726 and identified via mass spectros
168  biosynthetic pathway for DAP, the genome of F. nucleatum ATCC 25586 encodes a predicted DAP epimeras
169                             Co-incubation of F. nucleatum and Escherichia coli enhanced penetration o
170                                Inhibition of F. nucleatum host cell attachment and invasion with gala
171                A spontaneous mutant, lam, of F. nucleatum, isolated as defective in autoagglutination
172                             A DNA library of F. nucleatum FDC 364 was constructed by partial digestio
173                           Using a library of F. nucleatum mutants, we found that the Fap2 protein of
174                       Possible mechanisms of F. nucleatum's role in the pathogenesis of periodontal d
175 t was significantly lower than the number of F. nucleatum-positive subjects around teeth (P < 0.05).
176                                The number of F. nucleatum-positive subjects around the implant was si
177 ERT-2 epithelial cells with equal numbers of F. nucleatum and S. cristatus bacteria led to significan
178 albicans SN152 mutant library and a panel of F. nucleatum 23726 outer membrane protein mutants, we id
179 ortant for understanding the pathogenesis of F. nucleatum.
180         Although the phagocytosis pattern of F. nucleatum in the mixed infection remained similar to
181                   Neutrophil phagocytosis of F. nucleatum ssp. polymorphum was significantly greater
182                   Neutrophil phagocytosis of F. nucleatum ssp. polymorphum was significantly greater
183                   Neutrophil phagocytosis of F. nucleatum strains and neutrophil apoptosis were analy
184  cells may reflect the invasive phenotype of F. nucleatum and contribute to the greater pathogenic po
185 ibute to the greater pathogenic potential of F. nucleatum than of S. gordonii.
186                           In the presence of F. nucleatum, anaerobes persisted in high numbers (>10(7
187 sis of prevalence studies, the prevalence of F. nucleatum among 19 countries and B. fragilis among 10
188             In this study, the prevalence of F. nucleatum and B. fragilis among CRC patients has been
189 ur results emphasized the high prevalence of F. nucleatum and B. fragilis in CRC patients.
190 aled that Asia had the highest prevalence of F. nucleatum while most of the B. fragilis isolates in C
191 m mutants, we found that the Fap2 protein of F. nucleatum directly interacted with TIGIT, leading to
192  in which tumors exploit the Fap2 protein of F. nucleatum to inhibit immune cell activity via TIGIT.
193 tokines and CCL20 suggests the broad role of F. nucleatum and human antimicrobial peptides in primary
194 uld improve our understanding of the role of F. nucleatum in periodontal infections.
195  indicate that the immunosuppressive role of F. nucleatum is largely due to the ability of this organ
196 lated bone resorption and that the strain of F. nucleatum used appeared to be the strongest inducer o
197 e findings suggest that different strains of F. nucleatum impact neutrophil function in different way
198                               All strains of F. nucleatum significantly increased phagocytic capacity
199  with human and cynomolgus monkey strains of F. nucleatum.
200 l induction of hBD-2 by different strains of F. nucleatum; ATCC 25586 and ATCC 23726 induce significa
201 rphum was significantly greater than that of F. nucleatum ssp. polymorphum significantly blocked fMLP
202 rphum was significantly greater than that of F. nucleatum ssp. vincentii and ssp. nucleatum (P <0.001
203                        Given the ubiquity of F. nucleatum in the human mouth, these studies also sugg
204 obial infection underscored the virulence of F. nucleatum ssp polymorphum in particular with increase
205 path for anaerobic heme catabolism, offering F. nucleatum a competitive advantage in the colonization
206  species involved a heat-labile component on F. nucleatum and a mannan-containing heat-stable recepto
207  reappraisal of fusobacteria with a focus on F. nucleatum as a mutualist, infectious agent and oncoge
208 ached P. gingivalis but had no influences on F. nucleatum bacterial adherence.
209 valis simultaneously (at different sites) or F. nucleatum administered within 4 h prior to or 1 h fol
210                                     Overall, F. nucleatum and S. gordonii perturbed the gingival epit
211 he presence of any orange-complex pathogens (F. nucleatum, P. intermedia, and C. rectus), total cance
212 A may be a therapeutic target for preventing F. nucleatum colonization of the host.
213 ains, indicating that FAD-I is the principal F. nucleatum agent for hBD-2 induction in HOECs.
214 tivity, a diagnostic feature of BV, promoted F. nucleatum foraging and growth on mammalian sialoglyca
215                                 The purified F. nucleatum immunosuppressive protein (FIP) is composed
216  0.05), but no antibiotic was able to reduce F. nucleatum.
217  could be an effective strategy for reducing F. nucleatum-associated CRC metastasis.
218 ore, the yeast form of C. albicans repressed F. nucleatum-induced MCP-1 and TNFalpha production in ma
219  Casasanta et al show that CRC cell-resident F. nucleatum promotes cytokine secretion that may potent
220                     Hemagglutination of some F. nucleatum strains is also galactose sensitive, sugges
221                                  Strikingly, F. nucleatum achieves virulence in the absence of large,
222                               In this study, F. nucleatum was shown to activate both TLR2 and TLR4 in
223 e latter in the transwell assays, suggesting F. nucleatum may serve as an 'enabler' for other microor
224 ther of the other species in the peg system, F. nucleatum stimulated the growth of Veillonella sp. an
225                      Measuring and targeting F. nucleatum and its associated pathway will yield valua
226                              Thus, targeting F. nucleatum Fap2 or host epithelial Gal-GalNAc may redu
227               Recently, we demonstrated that F. nucleatum ATCC 23726 coaggregates with C. albicans SN
228 erleukin-6 (IL-6) and IL-8 demonstrated that F. nucleatum induced production of these cytokines, wher
229 tic and functional studies demonstrated that F. nucleatum promoted colorectal cancer resistance to ch
230 udies provided an initial demonstration that F. nucleatum adhered to and invaded HGEC and that this w
231 ments in mice also led to the discovery that F. nucleatum may also "give back" to the community by re
232  provides definitive molecular evidence that F. nucleatum adhesins play a vital role in inter-species
233 his study represents the first evidence that F. nucleatum may be transmitted hematogenously to the pl
234                                We found that F. nucleatum ATCC 23726 inhibits growth and hyphal morph
235                                We found that F. nucleatum infection induced both normal pancreatic ep
236 erless gene deletion approach and found that F. nucleatum invaded cultured HCT116 CRC cells through t
237                  These studies indicate that F. nucleatum aggregates PBMCs, and that this interaction
238                           Data indicate that F. nucleatum impaired endothelial cell proliferation and
239                  These studies indicate that F. nucleatum may facilitate the colonization of epitheli
240                   The findings indicate that F. nucleatum supports AUD through epigenetic regulation
241                 The data also indicated that F. nucleatum-induced cell apoptosis requires activation
242 tic analysis of sequence data indicates that F. nucleatum, F. necrophorum, and F. varium are the spec
243                We have shown previously that F. nucleatum adheres to and invades host epithelial and
244                 Thus, our findings show that F. nucleatum both directly and indirectly modulates immu
245         However, inhibitor studies show that F. nucleatum stimulation of hBD-2 mRNA requires both new
246                         These data show that F. nucleatum subspecies and T. forsythia synergistically
247  vaginal bacterial communities, we show that F. nucleatum supported robust outgrowth of Gardnerella v
248                Previously, it was shown that F. nucleatum induced preterm and term stillbirth in mice
249             Previous studies have shown that F. nucleatum species synergize with T. forsythia during
250                                          The F. nucleatum strain ATCC 25586 genome was assembled from
251           pHS17 was stably maintained in the F. nucleatum transformants, and differences in the trans
252 ine macrophage cell line, we showed that the F. nucleatum-induced inhibition of Candida hyphal morpho
253 erminal sequences of these proteins with the F. nucleatum genome revealed that the genes encoding the
254                   Our data support that this F. nucleatum-mediated inhibition is mediated by human, b
255                                        Thus, F. nucleatum infection in the pancreas elicits cytokine
256                                        Thus, F. nucleatum orchestrates a molecular network of the Tol
257 0018), to P. gingivalis (P = 0.0013), and to F. nucleatum (P = 0.0200) than women who delivered at te
258        In addition, polyclonal antibodies to F. nucleatum, which inhibited fusobacterial attachment t
259       Tumors from Apc(Min/+) mice exposed to F. nucleatum exhibit a proinflammatory expression signat
260 lecular level, the genetically transformable F. nucleatum strain ATCC 23726 was screened for adherenc
261 bled more than 70% long-term survival in two F. nucleatum-infected CRC models.
262 t the strong coaggregation between wild-type F. nucleatum 23726 and C. albicans SN152 in an in vitro
263 mors is inhibited in the presence of various F. nucleatum strains.
264                      We observed that viable F. nucleatum assembles biofilm-like structures in the tu
265                                         When F. nucleatum T18 was incubated with PHA-stimulated PBMCs
266 r the 6-month period in both groups, whereas F. nucleatum was significantly reduced in all visits in
267 release of bacterial-derived butyrate, while F. nucleatum and CRC cells are eliminated.
268                         This may explain why F. nucleatum is often found in mixed infections.
269 d C. albicans strains demonstrated CoAg with F. nucleatum.
270 ns grown at 37 degrees C to coaggregate with F. nucleatum.
271 ly C. dubliniensis strains coaggregated with F. nucleatum ATCC 49256 and no C. albicans strains showe
272 truction either alone or in combination with F. nucleatum.
273 were strong TLR4 agonists when combined with F. nucleatum LPS.
274 into neutrophil-like cells and cultured with F. nucleatum strains of subspecies (ssp.) nucleatum ATCC
275 incentii (FNV), and compare that genome with F. nucleatum ATCC 25586 (FN).
276                               Infection with F. nucleatum and P. gingivalis simultaneously (at differ
277 hort, high polygenic risk and infection with F. nucleatum have a small, yet independent impact on CHD
278                       Primary infection with F. nucleatum plus P. gingivalis at various ratios (i.e.,
279 116 cells was increased after infection with F. nucleatum; however, no species significantly altered
280  of gnotobiotic Drosophila melanogaster with F. nucleatum or supplementing the flies' diet with the S
281 an gingival epithelial cells stimulated with F. nucleatum cell wall extract, indicating possible invo
282 by immunofluorescence in HGE stimulated with F. nucleatum cell wall, consistent with induction of the
283 helium, in contrast to cultures treated with F. nucleatum clinical strain AHN, in which caspase-3 was
284 the polymicrobial consortium with or without F. nucleatum exhibited significantly increased alveolar

 
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