戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              P. gingivalis (ATCC 33277) was grown in broth culture, a
2                                              P. gingivalis colonization of the periodontal pockets ma
3                                              P. gingivalis did not increase Wnt3a mRNA levels, a find
4                                              P. gingivalis DPP5 was composed of 684 amino acids with
5                                              P. gingivalis has also been detected in human placentas
6                                              P. gingivalis IgG1 and IgG2 were analyzed.
7                                              P. gingivalis infection induced the expansion of three s
8                                              P. gingivalis is found on and within oral and gingival e
9                                              P. gingivalis LPS and AGE in combination caused signific
10                                              P. gingivalis secretes proteolytic gingipains (Kgp and R
11                                              P. gingivalis signature genes based on its activated eff
12                                              P. gingivalis utilizes protease-generated peptides deriv
13                                              P. gingivalis was associated with ACPAs (P = 0.04).
14                                              P. gingivalis-infected WT mice exhibited significantly i
15                                              P. gingivalis-NDK during infection inhibits extracellula
16 cetemcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. dentico
17 2X7 receptor expression was upregulated in a P. gingivalis oral infection model, and reduced IFN-gamm
18 rfere with the initiation and formation of a P. gingivalis-induced pathogenic community.
19  >75 IU/mL exhibited five-fold more abundant P. gingivalis levels than patients below the threshold.
20 oclasts and increased RANKL expression after P. gingivalis infection.
21 actate dehydrogenase release was found after P. gingivalis stimulation.
22                           Twelve hours after P. gingivalis stimulation, NZO osteoblasts showed signif
23  Simvastatin, being highly effective against P. gingivalis while not affecting commensal microbiota,
24  significant association between IgG against P. gingivalis and ACPAs in pre-RA and markers of RA acti
25                         In eRA, IgG2 against P. gingivalis was associated with ESR (P = 0.046) and AC
26  Smoking alters the humoral response against P. gingivalis and may increase P. gingivalis infectivity
27 like lipids) affords a mechanism that allows P. gingivalis to persist in homeostasis with its host.
28 nt reduction of A. actinomycetemcomitans and P. gingivalis counts (P > 0.05).
29 s was performed with combinations of AGE and P. gingivalis LPS.
30 +) cells, CD19(+) CD1d(hi) CD5(+) cells, and P. gingivalis-binding CD19(+) cells were significantly h
31 tionship between Streptococcus cristatus and P. gingivalis, and identified arginine deiminase (ArcA)
32  A direct physical contact between fungi and P. gingivalis was initiated via a modulation of gene exp
33  infection-induced eATP release in GECs, and P. gingivalis-NDK impacts this pathway.
34  correlation between the visfatin levels and P. gingivalis (r = 0.266, P <0.05), whereas no correlati
35 Although a trend for higher F. nucleatum and P. gingivalis concentrations in aCCP-positive patients w
36 ) between the number of cells in S phase and P. gingivalis invasion, the organism was more highly ass
37 ion of information on age, sex, smoking, and P. gingivalis results provided an area under the curve o
38 e expression profile induced by TNFalpha and P. gingivalis, suggesting a critical role for HDAC3 in G
39 inostat) significantly reduced TNFalpha- and P. gingivalis-inducible expression and/or production of
40        Saliva and serum were collected; anti-P. gingivalis salivary immunoglobulin A (IgA) and serum
41 alveolar bone loss, with a reduction in anti-P. gingivalis serum antibody titers compared with wild-t
42 monstrated alveolar bone loss and serum anti-P. gingivalis antibody titers equivalent to wild-type in
43 njection of collagen-antibody (ArthriomAb) + P. gingivalis, administration of Kava-205Me was able to
44 achment and enhanced exfoliation of attached P. gingivalis but had no influences on F. nucleatum bact
45 ibody activity specific to autocitrullinated P. gingivalis proteins.
46 ; which included all Socransky red bacteria (P. gingivalis, T. forsythia, T. denticola).
47  + CHX) and one positive correlation between P. gingivalis and nitrite at baseline (QS + CHX).
48  demonstrate that direct interaction between P. gingivalis and S. cristatus is necessary for the cell
49 activation of the uPA proteolytic cascade by P. gingivalis being required for the pathogen to induce
50 ta-Catenin activation in epithelial cells by P. gingivalis may contribute to a proliferative phenotyp
51                   The stimulatory effects by P. gingivalis-LPS were more evident when cells were cult
52 ested to counteract inflammation elicited by P. gingivalis In this study, the effects of A. muciniphi
53 ms driving aggressive progression of ESCC by P. gingivalis.
54 rding the subpopulations of MDSC expanded by P. gingivalis infection.
55 he Fim fimbriae, which are also expressed by P. gingivalis These results support a donor strand-based
56 truction of crestal alveolar bone induced by P. gingivalis colonization occurred regardless of the pr
57   Thus, the inflammatory response induced by P. gingivalis infection promotes the expansion of immune
58 +) Ly6C(++) subpopulation of MDSC induced by P. gingivalis infection was able to differentiate into o
59 -miR-2137 to control inflammation induced by P. gingivalis infection.
60 cci can antagonize the phenotypes induced by P. gingivalis, indicating functionally specialized roles
61  experimental periodontitis model induced by P. gingivalis-soaked ligatures.
62 ently reduced TNF-alpha secretion induced by P. gingivalis.
63  invasion of the aortic adventitial layer by P. gingivalis.
64 nt utilization of proteinaceous nutrients by P. gingivalis.
65 3beta were also proteolytically processed by P. gingivalis gingipains.
66 gly, we also discovered that SLs produced by P. gingivalis can be delivered to host cells independent
67 e outer membrane vesicles (OMVs) produced by P. gingivalis have been shown to play a role in periodon
68 o serine-glycine lipids are also produced by P. gingivalis The goal of this investigation was to dete
69 d extracellular polysaccharide production by P. gingivalis.
70    Part of the virulence factors secreted by P. gingivalis are the essential cysteine peptidases ging
71 induced IL-1beta processing and secretion by P. gingivalis-infected macrophages.
72  working hypothesis that synthesis of SLs by P. gingivalis is central to its ability to manipulate th
73 ein, we confirmed that APAF-1 is targeted by P. gingivalis in both cell types.
74 expression of TG2 with siRNA in HEp-2 cells, P. gingivalis association was greatly diminished.
75              Compared to non-infected cells, P. gingivalis infection decreased TEER (P < 0.0001) of H
76                               In conclusion, P. gingivalis infection induced infiltration of function
77                                 In contrast, P. gingivalis internalization and intracellular survival
78                                  Conversely, P. gingivalis infection-induced alveolar bone loss was a
79 Simvastatin was most efficient and decreased P. gingivalis counts more than 1,300-fold relative to th
80                     We recently demonstrated P. gingivalis-mediated gut barrier breakdown and exacerb
81                     In a dpp4-7-11-disrupted P. gingivalis ATCC 33277, a DPP7-like activity still rem
82  Amuc_1100 on macrophage polarization during P. gingivalis infection were evaluated in a murine model
83 es produced more A20 than WT cells following P. gingivalis challenge.
84  vivo abrogated alveolar bone loss following P. gingivalis infection.
85 ion of beta-catenin in the nucleus following P. gingivalis infection was confirmed by immunofluoresce
86 e of suture, have antimicrobial activity for P. gingivalis and E. faecalis.
87 ed that a protective environment existed for P. gingivalis within developed fungal biofilm formed und
88 resents an important pathogenesis factor for P. gingivalis.
89 -mediated activation of JAK2 is required for P. gingivalis-induced inflammatory cytokine production a
90 , we investigated another potential role for P. gingivalis in RA etiopathogenesis, based on the gener
91             Differences were significant for P. gingivalis, T. forsythia, T. denticola, P. micra, C.
92 lly, although the secretion of IL-1beta from P. gingivalis-infected macrophages was dependent on NLRP
93 nvestigate how lipopolysaccharide (LPS) from P. gingivalis stimulates bone resorption.
94 ata show, for the first time, that OMVs from P. gingivalis mediate increased vascular permeability, l
95 nt mice (Kit(W-sh/W-sh)) were protected from P. gingivalis-induced alveolar bone loss, with a reducti
96 ucture of the CTD of gingipain B (RgpB) from P. gingivalis, alone and together with a preceding immun
97                                 Furthermore, P. gingivalis augmented secretion and bioactivity of TGF
98 ured GECs or green-fluorescent-protein (GFP)-P. gingivalis-NDK transfected GECs revealed a perinuclea
99 d their effects on Porphyromonas gingivalis (P. gingivalis) elicited inflammation were evaluated in v
100 ency in myeloid cells also promotes a higher P. gingivalis lipopolysaccharide-induced inflammatory re
101  chronic in vitro infection model to test if P. gingivalis can induce DNA methylation in normal gingi
102                                           In P. gingivalis-infected BMMs, mmu-miR-155-5p significantl
103 d limited cell surface gingipain activity in P. gingivalis 381 renders this strain more immune-stimul
104 chondrial dehydrogenase activity but also in P. gingivalis-LPS-induced production of IL-6, TNF-alpha,
105                       Whether this change in P. gingivalis levels leads to biofilm alteration with re
106  the benefit appears to stem from changes in P. gingivalis levels in the DHA + aspirin treatment grou
107  production of pro-inflammatory cytokines in P. gingivalis-stimulated innate immune cells.
108      Increased bone loss was demonstrated in P. gingivalis-infected SOCS-3-knockout mice as compared
109 on abrogated periodontal bone destruction in P. gingivalis-infected, IL-33-treated mice.
110                 No significant difference in P. gingivalis attachment was noted among the corroded gr
111 lls, reduces expression of Wnt3a and Dvl3 in P. gingivalis-infected gingival tissues, and increases d
112 lectively alter virulence gene expression in P. gingivalis, and PGN_0294 and PGN_0806 may serve as re
113  on mRNA levels of inflammatory mediators in P. gingivalis-infected GFs.
114 r results show a novel phenomenon present in P. gingivalis-induced FGR, with relevance to human disea
115 ponse against P. gingivalis and may increase P. gingivalis infectivity, strengthening the evidence th
116 ity in aged mice may contribute to increased P. gingivalis colonization following inoculation and inc
117 ll four tested statins efficiently inhibited P. gingivalis growth and significantly decreased the cum
118 ression and production of several well-known P. gingivalis virulence factors including fimbrial prote
119 ated with fluorescein isothiocyanate-labeled P. gingivalis, and phagocytosis was measured in a fluoro
120 de tissues and significantly (p < 0.01) less P. gingivalis-induced bone resorption compared with cont
121 led wild-type Porphyromonas gingivalis, live P. gingivalis protease-deficient mutant KDP128, and live
122 nd molars in the presence or absence of live P. gingivalis infection.
123                                          LPS P. gingivalis and Pam2 also up-regulated RANKL and osteo
124                                          LPS P. gingivalis and Pam2 robustly enhanced osteoclast form
125                                          LPS P. gingivalis stimulated mineral release and matrix degr
126                                          LPS P. gingivalis stimulated RANKL in parietal osteoblasts d
127                           The effects by LPS P. gingivalis and four other TLR2 ligands on bone resorp
128              These data demonstrate that LPS P. gingivalis stimulates periosteal osteoclast formation
129                     Uniquely among microbes, P. gingivalis secretes a PAD, termed PPAD (Porphyromonas
130    In our PDL progenitor cell culture model, P. gingivalis LPS increased H3K4me3 histone methylation
131 eared even more pronounced, by six-fold more P. gingivalis (P = 0.025), in patients with a DAS-28 sco
132                                Using a novel P. gingivalis W50 PPAD mutant strain, incapable of prote
133  or microbiome that influence the ability of P. gingivalis to colonize the placenta may drive differe
134 lly, SAPP was able to impinge the ability of P. gingivalis to dysregulate innate immunity by repressi
135 iodontitis model, we assessed the ability of P. gingivalis to produce ISAR and FGR in Sprague Dawley
136  brain infections decreases the abundance of P. gingivalis DNA in brain and mitigates the neurotoxic
137 ABA) is required for maximal accumulation of P. gingivalis in dual-species communities.
138 ate significantly reduced growth activity of P. gingivalis, but not F. alocis, after therapy.
139 nstead correlated with increasing amounts of P. gingivalis DNA in the placentas of the C57BL/6J dams.
140                    Transcriptome analysis of P. gingivalis FLL366 revealed that approximately 11% of
141 -spectrometry method revealed association of P. gingivalis-NDK to the myosin-9 motor molecule.
142  which consequently increased the biomass of P. gingivalis in tri-species biofilms.
143 ce gingipain activity reduce the capacity of P. gingivalis 33277 to stimulate host cell innate immune
144                       Gingipains, a class of P. gingivalis proteases, are found in association with n
145 pletion led to greatly improved clearance of P. gingivalis.
146 crease oncogenic potential, and consortia of P. gingivalis and F. nucleatum are synergistically patho
147 ctive therapeutic targets for the control of P. gingivalis infections.
148                We investigated the effect of P. gingivalis on beta-catenin signaling, a major pathway
149 rain and mitigates the neurotoxic effects of P. gingivalis infection.
150 herefore, this study assessed the effects of P. gingivalis OMVs on the endothelium.
151 These data demonstrate that encapsulation of P. gingivalis plays a key role in the alveolar bone reso
152 cp has no effect on association and entry of P. gingivalis into human oral keratinocytes.
153                                  Evidence of P. gingivalis infiltration has been detected in autopsy
154 infected with P. gingivalis show evidence of P. gingivalis infiltration, along with various neuropath
155 ly, we find that in vivo clonal expansion of P. gingivalis-specific Th cells and induced regulatory T
156 t growth rate was not altered by exposure of P. gingivalis to SAPP, while monospecies and heterotypic
157 partner species that enhances the fitness of P. gingivalis while diminishing its virulence.
158 etabolize inulin but inhibited the growth of P. gingivalis and P. intermedia after 72 hours.
159  Bypassing LCs with systemic immunization of P. gingivalis resulted in a predominantly P. gingivalis-
160 eight in C57BL/6NCrl mice was independent of P. gingivalis in the placenta.
161 rmed fimbriae (pili) mediate interactions of P. gingivalis with other bacteria and with host cells th
162                    Intracellular invasion of P. gingivalis potentiated proliferation, migration, inva
163  as for caspase 1 activation irrespective of P. gingivalis fimbriae.
164 f A. actinomycetemcomitans or serotype K1 of P. gingivalis, higher levels of TLR2 or TLR4, respective
165 g/muL), sialidase (23 ng/muL), and levels of P. gingivalis (0.23%) and T. forsythia (0.35%), receiver
166                               Mean levels of P. gingivalis (r = 0.68), T. forsythia (r = 0.62), F. al
167                  Pre-rRNA and gDNA levels of P. gingivalis and F. alocis were quantified and compared
168                          Increased levels of P. gingivalis and F. nucleatum were associated with peri
169  young mice was linked to enhanced levels of P. gingivalis and reduced bacterial diversity.
170  testing such compounds in the management of P. gingivalis elicited inflammation, especially in the m
171 t could be exploited for the manipulation of P. gingivalis levels in oral communities and preventing
172 red for the peptide-fermenting metabolism of P. gingivalis.
173   Ultrastructural and confocal microscopy of P. gingivalis-co-cultured GECs or green-fluorescent-prot
174                 In vivo, in a mouse model of P. gingivalis-induced calvarial bone resorption, injecti
175                In vivo, in an acute model of P. gingivalis-induced calvarial destruction, administrat
176 esults, using conditional fimbria mutants of P. gingivalis, show that P. gingivalis infection of MoDC
177 s and two isogenic non-capsulated mutants of P. gingivalis, this study aimed to analyze whether P. gi
178 GPA) and DeltaPG0109-PG0118 (GPC) mutants of P. gingivalis.
179 uch and increases neutrophil phagocytosis of P. gingivalis in the transgenic animals; cutaneous fat d
180 vE1 increased the neutrophil phagocytosis of P. gingivalis in WT animals but had no impact in db/db a
181 egral importance of SLs in the physiology of P. gingivalis.
182 ether, the results indicate the potential of P. gingivalis to disrupt the control system of KLKs, pro
183           The local and systemic presence of P. gingivalis DNA was also monitored by polymerase chain
184 ew insight into the biological properties of P. gingivalis LPS lipid A moiety that could critically m
185  of this peptide on phenotypic properties of P. gingivalis related to virulence potential.
186                      Two surface proteins of P. gingivalis, PGN_0294 and PGN_0806, were found to inte
187                            The P:G ratios of P. gingivalis and F. alocis were compared and a low-stre
188 portant role of PDLSCs in the recognition of P. gingivalis, paracrine recruitment and activation of a
189 omplex abrogated the tumor-promoting role of P. gingivalis.
190                                The spread of P. gingivalis from the oral cavity to the reproductive t
191 apsular-defective knockout mutant strains of P. gingivalis induced less alveolar bone resorption than
192 84 or non-encapsulated ATCC 33277 strains of P. gingivalis were used as controls.
193 A increased the colonization and survival of P. gingivalis in a murine oral infection model.
194 mmensal bacterium, inhibited the survival of P. gingivalis in dual-species biofilms via the secretion
195 ptosome and XIAP as intracellular targets of P. gingivalis, contributing to the deterioration of peri
196                    We show that treatment of P. gingivalis with peptides corresponding to the conserv
197                           IL-33 treatment of P. gingivalis-infected mice significantly exacerbated al
198  contributes further to our understanding of P. gingivalis-induced modulation of miRNAs and their phy
199 study, we sought to explore the virulence of P. gingivalis (Pg) affecting glycogen synthase kinase 3
200                             The virulence of P. gingivalis likely reflects an alteration in the lipid
201 1780, analyzed the impact of SPT deletion on P. gingivalis gene expression (RNA-Seq analysis), and be
202           The effect of cell cycle phases on P. gingivalis invasion was measured by using antibiotic
203      Here we identify gingipains as the only P. gingivalis proteases responsible for SPINK6 degradati
204 ent serotypes of A. actinomycetemcomitans or P. gingivalis is TLR2 or TLR4 dependent, respectively.
205 ent serotypes of A. actinomycetemcomitans or P. gingivalis is Toll-like receptor 2 (TLR2) and/or TLR4
206 ) with different A. actinomycetemcomitans or P. gingivalis serotypes in the presence or absence of an
207 regardless of the presence of mucosal LCs or P. gingivalis-specific Th17 cells.
208 compared to that in sham-infected WT mice or P. gingivalis-infected TLR9(-/-) mice, which were resist
209                                Key pathogens P. gingivalis, T. forsythia, T. denticola, P. micra, C.
210 us mitis biofilm when the periodontopathogen P. gingivalis is present.
211 sion between mice treated with ligation plus P. gingivalis infection and mice treated with ligation a
212 of P. gingivalis resulted in a predominantly P. gingivalis-specific Th1 response regardless of whethe
213   Moreover, deletion of PPAD did not prevent P. gingivalis-mediated intestinal barrier breakdown and
214      CX3CR1(hi) monocyte/macrophages promote P. gingivalis survival by downregulating neutrophil phag
215                                   In pre-RA, P. gingivalis-specific IgG2 was associated with ACPAs (P
216 ciniphila or Amuc_1100 significantly reduced P. gingivalis-induced alveolar bone loss.
217 ith the function of Mfa fimbriae by reducing P. gingivalis adhesion to Streptococcus gordonii in a du
218 nsidered as an effective method for reducing P. gingivalis biofilm on implant surfaces, while being s
219 ate immune responses to these highly related P. gingivalis strains.
220                    The combination of saliva P. gingivalis quantity with pathogen-specific host respo
221 eptide array analysis, we identified several P. gingivalis-binding sites of ArcA, which led to the di
222                        Of the three species, P. gingivalis was reduced in both reservoirs 4-6 wk afte
223   Finally, pan-HDACi and HDAC3/6i suppressed P. gingivalis-induced expression of IL1B, CCL2, CCL5, CX
224  of tailored next-generation drugs to tackle P. gingivalis.
225                                    Targeting P. gingivalis or its activated effectors may provide nov
226            The present data demonstrate that P. gingivalis downregulates proliferation and promotes a
227               These results demonstrate that P. gingivalis synthesizes glycine lipids and that these
228 mokine receptor knockout mice and found that P. gingivalis clearance is significantly improved in the
229  Based on these results, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown
230                 Thus, our data indicate that P. gingivalis can induce the noncanonical activation of
231 istent with previous reports indicating that P. gingivalis invasion of cells is mediated by alpha5 in
232               In vitro, it was observed that P. gingivalis targets APAF-1, XIAP, caspase-3, and caspa
233  fimbria mutants of P. gingivalis, show that P. gingivalis infection of MoDCs induces an angiogenic m
234                      We recently showed that P. gingivalis can dampen eATP-induced IL-1beta secretion
235      A luciferase reporter assay showed that P. gingivalis increased the activity of the beta-catenin
236             Previous studies have shown that P. gingivalis accelerates the cell cycle and prevents ap
237     This study shows for the first time that P. gingivalis preferentially associates with and invades
238                                          The P. gingivalis fimbriae are assembled via a novel mechani
239 K1, and AKT were selectively degraded by the P. gingivalis lysine-specific gingipain (Kgp) in human e
240 onor strand-based assembly mechanism for the P. gingivalis fimbriae and demonstrate the feasibility o
241 nt on the nrfAH operon are also found in the P. gingivalis genome, we show that their gene products p
242 ed whether autocitrullinated proteins in the P. gingivalis proteome serve as cross-activation targets
243 d, confirming the requirement of TLR2 in the P. gingivalis-mediated inflammatory response.
244 e of a novel polymerization mechanism of the P. gingivalis fimbriae.
245 phenotype subset in the CCL2 MP group of the P. gingivalis-induced model.
246 anism and central roles in pathogenesis, the P. gingivalis fimbriae are attractive targets for anti-i
247                            At the same time, P. gingivalis-soaked ligatures were placed subgingivally
248 nction had greater production of antibody to P. gingivalis, greater IL-12 expression, and more plasma
249 ese data reveal a multidimensional aspect to P. gingivalis-S. gordonii interactions and establish pAB
250 ytokine response of oral epithelial cells to P. gingivalis.
251 e of elevated PA or OA levels and exposed to P. gingivalis.
252 at IRF6 is likely to promote inflammation to P. gingivalis through its regulation of IL-36gamma.
253 ly expressed in dysfunctional cells prior to P. gingivalis stimulation, the cytokine expression was i
254 showed an augmented inflammatory response to P. gingivalis in the presence of hyperlipidemic PA level
255 ) and increased in all groups in response to P. gingivalis inoculation (P < 0.01), whereas bone remod
256 tokine production in WT cells in response to P. gingivalis, thereby implicating TLR9 in inflammatory
257 -1 family cytokine IL-36gamma in response to P. gingivalis.
258  of proinflammatory cytokines in response to P. gingivalis.
259 ng differentiation of Th17 cells specific to P. gingivalis.
260 ing lymph nodes were higher in IL-33-treated P. gingivalis-infected mice versus phosphate buffered sa
261 ice versus phosphate buffered saline-treated P. gingivalis-infected controls (all P < 0.001).
262 ion of ACPA through the activity of a unique P. gingivalis peptidylarginine deiminase (PPAD) produced
263 xpressing diminished cytokine signaling upon P. gingivalis stimulation.
264                             Here, we utilize P. gingivalis mutant strains to show that pathogen-diffe
265                In addition, using an in vivo P. gingivalis-mediated periodontal disease model, we sho
266 givalis, this study aimed to analyze whether P. gingivalis encapsulation induces more severe alveolar
267  this investigation was to determine whether P. gingivalis produces additional lipid classes similar
268 Hcp appears to be the primary means by which P. gingivalis responds to NO(2) (-)-based stress.
269 eal a new host-pathogen interaction in which P. gingivalis activates a critical host proteolytic path
270  effect was observed in fibroblasts in which P. gingivalis increased cell death and apoptosis.
271 cristatus as the signaling molecule to which P. gingivalis responds by repressing the expression and
272 re found to be higher in individuals in whom P. gingivalis was detected than for those without P. gin
273  Infection of gingival epithelial cells with P. gingivalis did not influence the phosphorylation stat
274 ic treatment of normal epithelial cells with P. gingivalis introduced de novo DNA methylation within
275  in the oral cavity following challenge with P. gingivalis Our findings provide an explanation for ba
276 n oral epithelial cells were challenged with P. gingivalis.
277 xpressed more proteins during coculture with P. gingivalis W83 than with P. gingivalis 33277.
278 fected SOCS-3-knockout mice as compared with P. gingivalis-infected WT mice by direct morphologic mea
279 Wnt3a mRNA levels, a finding consistent with P. gingivalis-induced proteolytic processing causing the
280                       Mice were gavaged with P. gingivalis alone or in combination with A. muciniphil
281 matory cytokine IL-10 after incubations with P. gingivalis and F. nucleatum, as well as significantly
282 ges (BMM) and THP-1 cells were infected with P. gingivalis (MOI = 20:1) and a panel of cytokines were
283 row and spleen cells from mice infected with P. gingivalis and controls for surface expression of CD1
284 -engrafted Kit(W-sh/W-sh) mice infected with P. gingivalis demonstrated alveolar bone loss and serum
285 phages from A20-deficient mice infected with P. gingivalis displayed increased NF-kappaB activity and
286        Primary HGEp cells were infected with P. gingivalis either in the presence or absence of the n
287 bserved in the gingiva of mice infected with P. gingivalis in a periodontitis oral gavage model.
288      The brains of mice orally infected with P. gingivalis show evidence of P. gingivalis infiltratio
289 ne destruction following oral infection with P. gingivalis Mast cell-deficient mice (Kit(W-sh/W-sh))
290 e model of pregnancy and oral infection with P. gingivalis, C57BL/6J mice developed low fetal weight,
291 in determining the outcome of infection with P. gingivalis.
292 nolase, as partners for the interaction with P. gingivalis.
293               Strategies that interfere with P. gingivalis colonization and expression of virulence f
294                          PRP interfered with P. gingivalis and A. actinomycetemcomitans attachment an
295 g at week 10, mice were infected orally with P. gingivalis (W50) or placebo to induce alveolar bone l
296  control C57BL/6J mice, were stimulated with P. gingivalis.
297 g coculture with P. gingivalis W83 than with P. gingivalis 33277.
298 s CpG compared to those in mice treated with P. gingivalis LPS or CpG alone.
299  significantly increased with treatment with P. gingivalis LPS plus CpG compared to those in mice tre
300 ngivalis was detected than for those without P. gingivalis (P <0.01).

 
Page Top