ライフサイエンスコーパス: gingivalis

1 family cytokine IL-36gamma in response to P. gingivalis.

2 cies, Streptococcus mutans and Porphyromonas gingivalis.

3 tion led to greatly improved clearance of P. gingivalis.

4 ral epithelial cells were challenged with P. gingivalis.

5 f elevated PA or OA levels and exposed to P. gingivalis.

6 kine response of oral epithelial cells to P. gingivalis.

7 pportunistic pathogens such as Porphyromonas gingivalis.

8 for the peptide-fermenting metabolism of P. gingivalis.

9 ntrol C57BL/6J mice, were stimulated with P. gingivalis.

10 vasion of the aortic adventitial layer by P. gingivalis.

11 ents an important pathogenesis factor for P. gingivalis.

12 whose main infective agent is Porphyromonas gingivalis.

13 proinflammatory cytokines in response to P. gingivalis.

14 xtracellular polysaccharide production by P. gingivalis.

15 determining the outcome of infection with P. gingivalis.

16 differentiation of Th17 cells specific to P. gingivalis.

17 uL), sialidase (23 ng/muL), and levels of P. gingivalis (0.23%) and T. forsythia (0.35%), receiver op

18 emcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola,

19 emcomitans (MT4/MSP: 42%/36%), Porphyromonas gingivalis (78%/66%), Tannerella forsythia (98%/84%), Tr

20 Porphyromonas gingivalis, a key periodontal pathogen, is capable of in

21 ritoneal infection model using Porphyromonas gingivalis, a keystone pathogen for periodontitis, revea

22 e in eliciting inflammation to Porphyromonas gingivalis, a keystone pathogen in periodontitis.

23 Porphyromonas gingivalis, a major etiologic agent of periodontitis, ha

24 10(9) colony-forming units of Porphyromonas gingivalis A7436 through an oral gavage model for period

25 Previous studies have shown that P. gingivalis accelerates the cell cycle and prevents apopt

26 a new host-pathogen interaction in which P. gingivalis activates a critical host proteolytic pathway

27 st three periodontal bacteria: Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and F

28 Levels of Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevo

29 ure of the CTD of gingipain B (RgpB) from P. gingivalis, alone and together with a preceding immunogl

30 g enzymes in the oral pathogen Porphyromonas gingivalis Although a number of subunits of the T9SS hav

31 Porphyromonas gingivalis,an anaerobic bacterium strongly linked to inf

32 PRP interfered with P. gingivalis and A. actinomycetemcomitans attachment and e

33 gnificant association between IgG against P. gingivalis and ACPAs in pre-RA and markers of RA activit

34 riodontal pathogens, including Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, we

35 and spleen cells from mice infected with P. gingivalis and controls for surface expression of CD11b,

36 f suture, have antimicrobial activity for P. gingivalis and E. faecalis.

37 Porphyromonas gingivalis and especially Prevotella intermedius/nigresc

38 The P:G ratios of P. gingivalis and F. alocis were compared and a low-strengt

39 Pre-rRNA and gDNA levels of P. gingivalis and F. alocis were quantified and compared us

40 Porphyromonas gingivalis and Filifactor alocis are fastidious anaerobi

41 The effects by LPS P. gingivalis and four other TLR2 ligands on bone resorptio

42 induced by oral inoculation of Porphyromonas gingivalis and Fusobacterium nucleatum in young (4 to 5

43 not statistically significant, Porphyromonas gingivalis and Fusobacterium nucleatum occur in higher c

44 oking alters the humoral response against P. gingivalis and may increase P. gingivalis infectivity, s

45 CHX) and one positive correlation between P. gingivalis and nitrite at baseline (QS + CHX).

46 LPS P. gingivalis and Pam2 also up-regulated RANKL and osteocla

47 LPS P. gingivalis and Pam2 robustly enhanced osteoclast formati

48 tions of periodontal pathogens Porphyromonas gingivalis and Prevotella nigrescens induced periodontit

49 d cluster score (that included Porphyromonas gingivalis and Prevotella spp.) was positively associate

50 ung mice was linked to enhanced levels of P. gingivalis and reduced bacterial diversity.

51 monstrate that direct interaction between P. gingivalis and S. cristatus is necessary for the cell-ce

52 complex periodontal pathogens (Porphyromonas gingivalis and Tannerella forsythia), and cancer risk we

53 egative oral bacteria, such as Porphyromonas gingivalis and Tannerella forsythia, use disulfide bonds

54 The keystone pathogen Porphyromonas gingivalis and the accessory pathogen Streptococcus gord

55 The periodontal pathogen Porphyromonas gingivalis and the endodontic species Enterococcus faeca

56 inhibitable coaggregation with Porphyromonas gingivalis and were defective in cell binding.

57 of Pseudomonas aeruginosa and Porphyromonas gingivalis, and enables its antimicrobial activity despi

58 nship between Streptococcus cristatus and P. gingivalis, and identified arginine deiminase (ArcA) of

59 tively alter virulence gene expression in P. gingivalis, and PGN_0294 and PGN_0806 may serve as recep

60 d with fluorescein isothiocyanate-labeled P. gingivalis, and phagocytosis was measured in a fluorochr

61 strated alveolar bone loss and serum anti-P. gingivalis antibody titers equivalent to wild-type infec

62 1, of the periodontal pathogen Porphyromonas gingivalis are responsible for adherence to other bacter

63 ion of neutrophil responses by Porphyromonas gingivalis as a mechanism that contributes to forming a

64 e colonizer pathogens, such as Porphyromonas gingivalis, as the biofilm ages and periodontal inflamma

65 ression of TG2 with siRNA in HEp-2 cells, P. gingivalis association was greatly diminished.

66 In a dpp4-7-11-disrupted P. gingivalis ATCC 33277, a DPP7-like activity still remain

67 No significant difference in P. gingivalis attachment was noted among the corroded group

68 ivation of the uPA proteolytic cascade by P. gingivalis being required for the pathogen to induce alv

69 cells, CD19(+) CD1d(hi) CD5(+) cells, and P. gingivalis-binding CD19(+) cells were significantly high

70 ide array analysis, we identified several P. gingivalis-binding sites of ArcA, which led to the disco

71 ment and enhanced exfoliation of attached P. gingivalis but had no influences on F. nucleatum bacteri

72 significantly reduced growth activity of P. gingivalis, but not F. alocis, after therapy.

73 We recently showed that P. gingivalis can dampen eATP-induced IL-1beta secretion by

74 ronic in vitro infection model to test if P. gingivalis can induce DNA methylation in normal gingival

75 Thus, our data indicate that P. gingivalis can induce the noncanonical activation of bet

76 itis-associated oral bacterium Porphyromonas gingivalis, can subvert host immunity to remodel a norma

77 produced more A20 than WT cells following P. gingivalis challenge.

78 ine receptor knockout mice and found that P. gingivalis clearance is significantly improved in the ab

79 ltrastructural and confocal microscopy of P. gingivalis-co-cultured GECs or green-fluorescent-protein

80 Strategies that interfere with P. gingivalis colonization and expression of virulence fact

81 in aged mice may contribute to increased P. gingivalis colonization following inoculation and increa

82 ction of crestal alveolar bone induced by P. gingivalis colonization occurred regardless of the prese

83 P. gingivalis colonization of the periodontal pockets may i

84 hough a trend for higher F. nucleatum and P. gingivalis concentrations in aCCP-positive patients with

85 some and XIAP as intracellular targets of P. gingivalis, contributing to the deterioration of periodo

86 est effect of DHA + aspirin on Porphyromonas gingivalis counts was associated with 14% (95% confidenc

87 mplex-KCNK1, p = 3.4 x 10(-7); Porphyromonas gingivalis-DAB2IP, p = 1.0 x 10(-6)).

88 ich the opportunistic pathogen Porphyromonas gingivalis dampens innate immune responses by disruption

89 grafted Kit(W-sh/W-sh) mice infected with P. gingivalis demonstrated alveolar bone loss and serum ant

90 P. gingivalis did not increase Wnt3a mRNA levels, a finding

91 fection of gingival epithelial cells with P. gingivalis did not influence the phosphorylation status

92 The local and systemic presence of P. gingivalis DNA was also monitored by polymerase chain re

93 The present data demonstrate that P. gingivalis downregulates proliferation and promotes apop

94 P. gingivalis DPP5 was composed of 684 amino acids with a m

95 duced by the keystone pathogen Porphyromonas gingivalis, dramatically increased their ability to degr

96 erium nucleatum ATCC10953, and Porphyromonas gingivalis DSM20709) were placed in a series of IMC ampo

97 . naeslundii I, Actinomyces gerencseriae, C. gingivalis, E. corrodens, C. concisus, Prevotella nigres

98 caused by oral infection with Porphyromonas gingivalis enhances articular bone loss.

99 f a novel polymerization mechanism of the P. gingivalis fimbriae.

100 for caspase 1 activation irrespective of P. gingivalis fimbriae.

101 Transcriptome analysis of P. gingivalis FLL366 revealed that approximately 11% of the

102 ta were also proteolytically processed by P. gingivalis gingipains.

103 ion had greater production of antibody to P. gingivalis, greater IL-12 expression, and more plasma ce

104 Porphyromonas gingivalis has orthologs for each of these that are requ

105 cter actinomycetemcomitans and Porphyromonas gingivalis have been shown to induce differential dendri

106 sized that histatin 5 binds to Porphyromonas gingivalis hemagglutinin B (HagB) and attenuates HagB-in

107 . actinomycetemcomitans or serotype K1 of P. gingivalis, higher levels of TLR2 or TLR4, respectively,

108 P. gingivalis IgG1 and IgG2 were analyzed.

109 ncreased the colonization and survival of P. gingivalis in a murine oral infection model.

110 rved in the gingiva of mice infected with P. gingivalis in a periodontitis oral gavage model.

111 , we confirmed that APAF-1 is targeted by P. gingivalis in both cell types.

112 ) is required for maximal accumulation of P. gingivalis in dual-species communities.

113 bulin (Ig)G subclasses against Porphyromonas gingivalis in individuals with pre-RA and eRA were compa

114 of RvE1 on the phagocytosis of Porphyromonas gingivalis in T2D.

115 wed an augmented inflammatory response to P. gingivalis in the presence of hyperlipidemic PA levels a

116 and increases neutrophil phagocytosis of P. gingivalis in the transgenic animals; cutaneous fat depo

117 increased the neutrophil phagocytosis of P. gingivalis in WT animals but had no impact in db/db anim

118 (lipopolysaccharide [LPS] from Porphyromonas gingivalis) in a manner consistent with the clinical obs

119 fect was observed in fibroblasts in which P. gingivalis increased cell death and apoptosis.

120 A luciferase reporter assay showed that P. gingivalis increased the activity of the beta-catenin-de

121 mice (Kit(W-sh/W-sh)) were protected from P. gingivalis-induced alveolar bone loss, with a reduction

122 tissues and significantly (p < 0.01) less P. gingivalis-induced bone resorption compared with control

123 In vivo, in a mouse model of P. gingivalis-induced calvarial bone resorption, injection

124 diated activation of JAK2 is required for P. gingivalis-induced inflammatory cytokine production and

125 els on alveolar bone loss in a Porphyromonas gingivalis-induced model of periodontal disease and to a

126 ntributes further to our understanding of P. gingivalis-induced modulation of miRNAs and their physio

127 re with the initiation and formation of a P. gingivalis-induced pathogenic community.

128 controls in a murine model of Porphyromonas gingivalis-induced periodontitis and report the first in

129 in distinct models, including Porphyromonas gingivalis-induced periodontitis, ligature-induced perio

130 3a mRNA levels, a finding consistent with P. gingivalis-induced proteolytic processing causing the in

131 sed on these results, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown mec

132 gent of chronic periodontitis, Porphyromonas gingivalis, infect blood myeloid dendritic cells (mDCs).

133 In P. gingivalis-infected BMMs, mmu-miR-155-5p significantly d

134 versus phosphate buffered saline-treated P. gingivalis-infected controls (all P < 0.001).

135 , although the secretion of IL-1beta from P. gingivalis-infected macrophages was dependent on NLRP3,

136 uced IL-1beta processing and secretion by P. gingivalis-infected macrophages.

137 gher in periodontal tissues of Porphyromonas gingivalis-infected mice as compared with sham-infected

138 IL-33 treatment of P. gingivalis-infected mice significantly exacerbated alveo

139 lymph nodes were higher in IL-33-treated P. gingivalis-infected mice versus phosphate buffered salin

140 Increased bone loss was demonstrated in P. gingivalis-infected SOCS-3-knockout mice as compared wit

141 pared to that in sham-infected WT mice or P. gingivalis-infected TLR9(-/-) mice, which were resistant

142 ted SOCS-3-knockout mice as compared with P. gingivalis-infected WT mice by direct morphologic measur

143 P. gingivalis-infected WT mice exhibited significantly incr

144 abrogated periodontal bone destruction in P. gingivalis-infected, IL-33-treated mice.

145 n between mice treated with ligation plus P. gingivalis infection and mice treated with ligation alon

146 In conclusion, P. gingivalis infection induced infiltration of functional/

147 P. gingivalis infection induced the expansion of three subp

148 mbria mutants of P. gingivalis, show that P. gingivalis infection of MoDCs induces an angiogenic migr

149 hus, the inflammatory response induced by P. gingivalis infection promotes the expansion of immune-su

150 Ly6C(++) subpopulation of MDSC induced by P. gingivalis infection was able to differentiate into oste

151 of beta-catenin in the nucleus following P. gingivalis infection was confirmed by immunofluorescence

152 Conversely, P. gingivalis infection-induced alveolar bone loss was atte

153 asts and increased RANKL expression after P. gingivalis infection.

154 vo abrogated alveolar bone loss following P. gingivalis infection.

155 molars in the presence or absence of live P. gingivalis infection.

156 R-2137 to control inflammation induced by P. gingivalis infection.

157 ng the subpopulations of MDSC expanded by P. gingivalis infection.

158 se against P. gingivalis and may increase P. gingivalis infectivity, strengthening the evidence that

159 nd increased in all groups in response to P. gingivalis inoculation (P < 0.01), whereas bone remodeli

160 treatment of normal epithelial cells with P. gingivalis introduced de novo DNA methylation within the

161 ent with previous reports indicating that P. gingivalis invasion of cells is mediated by alpha5 integ

162 The effect of cell cycle phases on P. gingivalis invasion was measured by using antibiotic pro

163 etween the number of cells in S phase and P. gingivalis invasion, the organism was more highly associ

164 Porphyromonas gingivalis is a keystone pathogen that contributes to pe

165 Porphyromonas gingivalis is a keystone periodontal pathogen and its li

166 Porphyromonas gingivalis is a member of the human oral microbiome abun

167 Porphyromonas gingivalis is a peptide-fermenting asaccharolytic period

168 Porphyromonas gingivalis is a predominant pathogen that maintains chro

169 Porphyromonas gingivalis is able to invade and modulate host-immune re

170 Porphyromonas gingivalis is an established pathogen in periodontal dis

171 Porphyromonas gingivalis is considered a keystone pathogen in the dise

172 P. gingivalis is found on and within oral and gingival epit

173 Porphyromonas gingivalis is intimately associated with periodontitis a

174 mitis biofilm when the periodontopathogen P. gingivalis is present.

175 Porphyromonas gingivalis is the major causative agent of periodontitis

176 serotypes of A. actinomycetemcomitans or P. gingivalis is TLR2 or TLR4 dependent, respectively.

177 serotypes of A. actinomycetemcomitans or P. gingivalis is Toll-like receptor 2 (TLR2) and/or TLR4 de

178 periodontal pathogens, such as Porphyromonas gingivalis, is expressed in the context of this polymicr

179 c infectious agents, including Porphyromonas gingivalis, is shown to drive-differentiation of monocyt

180 ould be exploited for the manipulation of P. gingivalis levels in oral communities and preventing rea

181 e benefit appears to stem from changes in P. gingivalis levels in the DHA + aspirin treatment group.

182 Whether this change in P. gingivalis levels leads to biofilm alteration with rever

183 The virulence of P. gingivalis likely reflects an alteration in the lipid A

184 Porphyromonas gingivalis lipid A heterogeneity modulates cytokine expr

185 7BL/6J mice were cultured with Porphyromonas gingivalis lipopolysaccharide (LPS) and cytosine-phospho

186 in the presence and absence of Porphyromonas gingivalis lipopolysaccharide (LPS) on IL-6, IL-8, and C

187 in constitutively released or Porphyromonas gingivalis lipopolysaccharide (PgLPS)-stimulated epithel

188 y in myeloid cells also promotes a higher P. gingivalis lipopolysaccharide-induced inflammatory respo

189 ation by heat-killed wild-type Porphyromonas gingivalis, live P. gingivalis protease-deficient mutant

190 P. gingivalis LPS and AGE in combination caused significant

191 insight into the biological properties of P. gingivalis LPS lipid A moiety that could critically modu

192 pG compared to those in mice treated with P. gingivalis LPS or CpG alone.

193 gnificantly increased with treatment with P. gingivalis LPS plus CpG compared to those in mice treate

194 as performed with combinations of AGE and P. gingivalis LPS.

195 The stimulatory effects by P. gingivalis-LPS were more evident when cells were culture

196 ndrial dehydrogenase activity but also in P. gingivalis-LPS-induced production of IL-6, TNF-alpha, or

197 and AKT were selectively degraded by the P. gingivalis lysine-specific gingipain (Kgp) in human endo

198 destruction following oral infection with P. gingivalis Mast cell-deficient mice (Kit(W-sh/W-sh)) wer

199 periodontal bacteria, such as Porphyromonas gingivalis Mast cells are sentinels at mucosal surfaces

200 Catenin activation in epithelial cells by P. gingivalis may contribute to a proliferative phenotype.

201 confirming the requirement of TLR2 in the P. gingivalis-mediated inflammatory response.

202 Here, we utilize P. gingivalis mutant strains to show that pathogen-differen

203 P. gingivalis-NDK during infection inhibits extracellular-A

204 fection-induced eATP release in GECs, and P. gingivalis-NDK impacts this pathway.

205 ectrometry method revealed association of P. gingivalis-NDK to the myosin-9 motor molecule.

206 d GECs or green-fluorescent-protein (GFP)-P. gingivalis-NDK transfected GECs revealed a perinuclear/c

207 We investigated the effect of P. gingivalis on beta-catenin signaling, a major pathway in

208 dy is to analyze the effect of Porphyromonas gingivalis on differentiation of primary osteoblasts fro

209 receptor expression was upregulated in a P. gingivalis oral infection model, and reduced IFN-gamma a

210 the oral cavity following challenge with P. gingivalis Our findings provide an explanation for bacte

211 valis was detected than for those without P. gingivalis (P <0.01).

212 Porphyromonas gingivalis (P.g.)-induced TNF-alpha can be affected by m

213 Porphyromonas gingivalis (Pg) capsule enables evasion from phagocytosi

214 presented greater reduction of Porphyromonas gingivalis (Pg) DNA counts at 6 months (P = 0.0001).

215 Porphyromonas gingivalis (Pg) is a keystone pathogen in the aetiology

216 Porphyromonas gingivalis (Pg) is a major periodontal pathogen that con

217 sed to determine the effect of Porphyromonas gingivalis (Pg) LPS on insulin secretion.

218 er actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Campylobacter rectus (Cr), and Tannerel

219 consisting of species such as Porphyromonas gingivalis (Pg), in the etiology of peri-implantitis.

220 ith the submucosal presence of Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Tannerella

221 analysis of bacterial DNA for Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Treponema d

222 ifically regarding the role of Porphyromonas gingivalis (Pg).

223 man monocyte THP-1 to LPS from Porphyromonas gingivalis (PgLPS), an oral microbe implicated in the pa

224 Two surface proteins of P. gingivalis, PGN_0294 and PGN_0806, were found to interac

225 This study shows for the first time that P. gingivalis preferentially associates with and invades ce

226 and include organisms such as Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleat

227 and the presence and levels of Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens

228 s, the Gram-negative bacterium Porphyromonas gingivalis, produces a vast arsenal of virulence factors

229 wild-type Porphyromonas gingivalis, live P. gingivalis protease-deficient mutant KDP128, and live Ag

230 Here we identify gingipains as the only P. gingivalis proteases responsible for SPINK6 degradation.

231 The combination of saliva P. gingivalis quantity with pathogen-specific host response

232 rrelation between the visfatin levels and P. gingivalis (r = 0.266, P <0.05), whereas no correlation

233 Mean levels of P. gingivalis (r = 0.68), T. forsythia (r = 0.62), F. aloci

234 this peptide on phenotypic properties of P. gingivalis related to virulence potential.

235 cter actinomycetemcomitans and Porphyromonas gingivalis, respectively.

236 status as the signaling molecule to which P. gingivalis responds by repressing the expression and pro

237 passing LCs with systemic immunization of P. gingivalis resulted in a predominantly P. gingivalis-spe

238 of information on age, sex, smoking, and P. gingivalis results provided an area under the curve of 0

239 data reveal a multidimensional aspect to P. gingivalis-S. gordonii interactions and establish pABA a

240 Saliva and serum were collected; anti-P. gingivalis salivary immunoglobulin A (IgA) and serum IgG

241 Uniquely among microbes, P. gingivalis secretes a PAD, termed PPAD (Porphyromonas pe

242 P. gingivalis secretes proteolytic gingipains (Kgp and RgpA

243 A key pathogen, Porphyromonas gingivalis, secretes gingipains, cysteine proteases impl

244 ith different A. actinomycetemcomitans or P. gingivalis serotypes in the presence or absence of anti-

245 eolar bone loss, with a reduction in anti-P. gingivalis serum antibody titers compared with wild-type

246 lts, using conditional fimbria mutants of P. gingivalis, show that P. gingivalis infection of MoDCs i

247 At the same time, P. gingivalis-soaked ligatures were placed subgingivally ar

248 perimental periodontitis model induced by P. gingivalis-soaked ligatures.

249 In pre-RA, P. gingivalis-specific IgG2 was associated with ACPAs (P =

250 we find that in vivo clonal expansion of P. gingivalis-specific Th cells and induced regulatory T ce

251 P. gingivalis resulted in a predominantly P. gingivalis-specific Th1 response regardless of whether L

252 ardless of the presence of mucosal LCs or P. gingivalis-specific Th17 cells.

253 LPS P. gingivalis stimulated mineral release and matrix degrada

254 LPS P. gingivalis stimulated RANKL in parietal osteoblasts depe

255 stigate how lipopolysaccharide (LPS) from P. gingivalis stimulates bone resorption.

256 These data demonstrate that LPS P. gingivalis stimulates periosteal osteoclast formation an

257 Twelve hours after P. gingivalis stimulation, NZO osteoblasts showed significa

258 expressed in dysfunctional cells prior to P. gingivalis stimulation, the cytokine expression was incr

259 essing diminished cytokine signaling upon P. gingivalis stimulation.

260 ate dehydrogenase release was found after P. gingivalis stimulation.

261 CX3CR1(hi) monocyte/macrophages promote P. gingivalis survival by downregulating neutrophil phagocy

262 Bacterial loads of Porphyromonas gingivalis, T. forsythia, Parvimonas micra, and total ba

263 Key pathogens P. gingivalis, T. forsythia, T. denticola, P. micra, C. rec

264 Differences were significant for P. gingivalis, T. forsythia, T. denticola, P. micra, C. rec

265 ied twenty-one OTUs, including Porphyromonas gingivalis, Tannerella forsythia and Filifactor alocis,

266 Levels of Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actino

267 g and levels of microorganisms Porphyromonas gingivalis, Tannerella forsythia, and Campylobacter rect

268 d subgingival plaque levels of Porphyromonas gingivalis, Tannerella forsythia, and Fusobacterium nucl

269 periodontal pathogens, such as Porphyromonas gingivalis, Tannerella forsythia, and Prevotella interme

270 s, Fretibacterium fastidiosum, Porphyromonas gingivalis, Tannerella forsythia, and Selenomonas sputig

271 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticol

272 T1 decreased the counts of Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia

273 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, a

274 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, S

275 In vitro, it was observed that P. gingivalis targets APAF-1, XIAP, caspase-3, and caspase-

276 was induced by infection with Porphyromonas gingivalis The expression of several miRNAs was modulate

277 In the periodontal pathogen Porphyromonas gingivalis, the CTD is cleaved off by PorU sortase in a

278 ponderance of bacteria such as Porphyromonas gingivalis, the main etiological agent of periodontitis.

279 ine production in WT cells in response to P. gingivalis, thereby implicating TLR9 in inflammatory res

280 IRF6 is likely to promote inflammation to P. gingivalis through its regulation of IL-36gamma.

281 er, the results indicate the potential of P. gingivalis to disrupt the control system of KLKs, provid

282 , SAPP was able to impinge the ability of P. gingivalis to dysregulate innate immunity by repressing

283 The adaptation of Porphyromonas gingivalis to H2O2-induced stress while inducible is mod

284 rowth rate was not altered by exposure of P. gingivalis to SAPP, while monospecies and heterotypic bi

285 ce of the periodontal pathogen Porphyromonas gingivalis trended with higher risk of ESCC.

286 to several species, including Porphyromonas gingivalis, Treponema denticola, and Campylobacter rectu

287 ence supporting association of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythi

288 cterial inoculum consisting of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythi

289 ments, rats were infected with Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythi

290 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythi

291 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, a

292 a polymicrobial consortium of Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, a

293 Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, a

294 sion and production of several well-known P. gingivalis virulence factors including fimbrial proteins

295 t week 10, mice were infected orally with P. gingivalis (W50) or placebo to induce alveolar bone loss

296 P. gingivalis was associated with ACPAs (P = 0.04).

297 In eRA, IgG2 against P. gingivalis was associated with ESR (P = 0.046) and ACPAs

298 found to be higher in individuals in whom P. gingivalis was detected than for those without P. gingiv

299 ed human periodontal pathogen, Porphyromonas gingivalis We found that oral mucosal LCs did not protec

300 tner species that enhances the fitness of P. gingivalis while diminishing its virulence.

301 cter actinomycetemcomitans and Porphyromonas gingivalis with extended NO-release kinetics at pH 7.4.