ライフサイエンスコーパス: gingivalis

1 from the periodontal pathogen Porphyromonas gingivalis.

2 ase, as partners for the interaction with P. gingivalis.

3 ) and DeltaPG0109-PG0118 (GPC) mutants of P. gingivalis.

4 tailored next-generation drugs to tackle P. gingivalis.

5 ly reduced TNF-alpha secretion induced by P. gingivalis.

6 ease is an anaerobic bacterium-Porphyromonas gingivalis.

7 al importance of SLs in the physiology of P. gingivalis.

8 xtracellular polysaccharide production by P. gingivalis.

9 determining the outcome of infection with P. gingivalis.

10 differentiation of Th17 cells specific to P. gingivalis.

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

12 lex abrogated the tumor-promoting role of P. gingivalis.

13 utilization of proteinaceous nutrients by P. gingivalis.

14 driving aggressive progression of ESCC by P. gingivalis.

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

16 gingipain activity reduce the capacity of P. gingivalis 33277 to stimulate host cell innate immune re

17 imited cell surface gingipain activity in P. gingivalis 381 renders this strain more immune-stimulato

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

19 action (qPCR) for detection of Porphyromonas gingivalis, a keystone pathogen and to assess the levels

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

21 A and periodontal disease, and Porphyromonas gingivalis, a known driver of periodontitis, has been pr

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

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

24 the function of Mfa fimbriae by reducing P. gingivalis adhesion to Streptococcus gordonii in a dual-

25 ction of collagen-antibody (ArthriomAb) + P. gingivalis, administration of Kava-205Me was able to red

26 Mice were gavaged with P. gingivalis alone or in combination with A. muciniphila o

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

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

29 Porphyromonas gingivalis, an asaccharolytic member of the Bacteroidete

30 ical virulence determinants of Porphyromonas gingivalis, an emerging Alzheimer's disease, cancer, and

31 ease, such as the link between Porphyromonas gingivalis and atherosclerosis.

32 ed by the periodontal pathogen Porphyromonas gingivalis and can be detected in lipid extracts of dise

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

34 Porphyromonas gingivalis and especially Prevotella intermedius/nigresc

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

36 ase oncogenic potential, and consortia of P. gingivalis and F. nucleatum are synergistically pathogen

37 Increased levels of P. gingivalis and F. nucleatum were associated with periodo

38 ory cytokine IL-10 after incubations with P. gingivalis and F. nucleatum, as well as significantly re

39 n of the periodontal pathogens Porphyromonas gingivalis and Fusobacterium nucleatum growth and attach

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

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

42 analysis of keystone pathogen Porphyromonas gingivalis and its consortium members Fusobacterium nucl

43 models through inoculation of Porphyromonas gingivalis and ligature around the murine molar.

44 bolize inulin but inhibited the growth of P. gingivalis and P. intermedia after 72 hours.

45 ther LS inhibits the growth of Porphyromonas gingivalis and Prevotella intermedia.

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

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

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

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

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

51 The recolonization of Porphyromonas gingivalis and Treponema denticola was reduced after adj

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

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

54 to a keystone oral bacterium, Porphyromonas gingivalis, and restrains periodontal inflammation throu

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

56 1, of the periodontal pathogen Porphyromonas gingivalis are responsible for adherence to other bacter

57 Part of the virulence factors secreted by P. gingivalis are the essential cysteine peptidases gingipa

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

59 P. gingivalis (ATCC 33277) was grown in broth culture, and

60 Furthermore, P. gingivalis augmented secretion and bioactivity of TGFbet

61 r, Fusobacterium nucleatum and Porphyromonas gingivalis, based on results from epidemiological as wel

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

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

64 dered as an effective method for reducing P. gingivalis biofilm on implant surfaces, while being safe

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

66 odel of pregnancy and oral infection with P. gingivalis, C57BL/6J mice developed low fetal weight, wh

67 , we also discovered that SLs produced by P. gingivalis can be delivered to host cells independent of

68 ibodies raised in mice against Porphyromonas gingivalis caused fetal loss in a mouse pregnancy model

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

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

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

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

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

74 reduction of A. actinomycetemcomitans and P. gingivalis counts (P > 0.05).

75 vastatin was most efficient and decreased P. gingivalis counts more than 1,300-fold relative to the c

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

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

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

79 d proinflammatory responses to Porphyromonas gingivalis-derived lipopolysaccharide in circulating neu

80 ges from A20-deficient mice infected with P. gingivalis displayed increased NF-kappaB activity and cy

81 ncreased in the RA group, only Porphyromonas gingivalis displayed significant correlations with plaqu

82 l epithelial (HGEp) cells with Porphyromonas gingivalis disrupts barrier function by inducing epigene

83 ain infections decreases the abundance of P. gingivalis DNA in brain and mitigates the neurotoxic eff

84 ead correlated with increasing amounts of P. gingivalis DNA in the placentas of the C57BL/6J dams.

85 Primary HGEp cells were infected with P. gingivalis either in the presence or absence of the non-

86 sting such compounds in the management of P. gingivalis elicited inflammation, especially in the mana

87 heir effects on Porphyromonas gingivalis (P. gingivalis) elicited inflammation were evaluated in vitr

88 alis, this study aimed to analyze whether P. gingivalis encapsulation induces more severe alveolar bo

89 with the periodontal pathogen Porphyromonas gingivalis enhances the activity of Janus kinase 3 (JAK3

90 r strand-based assembly mechanism for the P. gingivalis fimbriae and demonstrate the feasibility of u

91 The P. gingivalis fimbriae are assembled via a novel mechanism

92 sm and central roles in pathogenesis, the P. gingivalis fimbriae are attractive targets for anti-infe

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

94 ed in periodontitis, including Porphyromonas gingivalis, Fretibacterium fastidiosum, Filifactor aloci

95 aceae [G-1] bacterium HMT 113, Porphyromonas gingivalis, Fretibacterium fastidiosum, Filifactor aloci

96 The spread of P. gingivalis from the oral cavity to the reproductive trac

97 ted of five microbial species (Porphyromonas gingivalis, Fusobacterium nucleatum, Actinomyces naeslun

98 such as Streptococcus mutans, Porphyromonas gingivalis, Fusobacterium nucleatum, and Pseudomonas aer

99 and multi-species biofilms of Porphyromonas gingivalis, Fusobacterium nucleatum, and Streptococcus o

100 periodontal pathogens, such as Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denti

101 0, analyzed the impact of SPT deletion on P. gingivalis gene expression (RNA-Seq analysis), and began

102 , we compare a nearly complete Porphyromonas gingivalis genome to previously published genomes recove

103 on the nrfAH operon are also found in the P. gingivalis genome, we show that their gene products play

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

105 four tested statins efficiently inhibited P. gingivalis growth and significantly decreased the cumula

106 P. gingivalis has also been detected in human placentas ass

107 Encapsulation of Porphyromonas gingivalis has been demonstrated as responsible of sever

108 uter membrane vesicles (OMVs) produced by P. gingivalis have been shown to play a role in periodontit

109 P. gingivalis IgG1 and IgG2 were analyzed.

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

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

112 nsal bacterium, inhibited the survival of P. gingivalis in dual-species biofilms via the secretion of

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

114 e investigated another potential role for P. gingivalis in RA etiopathogenesis, based on the generati

115 ht in C57BL/6NCrl mice was independent of P. gingivalis in the placenta.

116 ed to counteract inflammation elicited by P. gingivalis In this study, the effects of A. muciniphila

117 ich consequently increased the biomass of P. gingivalis in tri-species biofilms.

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 can antagonize the phenotypes induced by P. gingivalis, indicating functionally specialized roles fo

121 ular-defective knockout mutant strains of P. gingivalis induced less alveolar bone resorption than th

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

123 iphila or Amuc_1100 significantly reduced P. gingivalis-induced alveolar bone loss.

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

125 In vivo, in an acute model of P. gingivalis-induced calvarial destruction, administration

126 inally, pan-HDACi and HDAC3/6i suppressed P. gingivalis-induced expression of IL1B, CCL2, CCL5, CXCL1

127 esults show a novel phenomenon present in P. gingivalis-induced FGR, with relevance to human disease

128 notype subset in the CCL2 MP group of the P. gingivalis-induced model.

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

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

131 stat) significantly reduced TNFalpha- and P. gingivalis-inducible expression and/or production of a c

132 Msx2 knock-in Swiss mice using Porphyromonas gingivalis infected ligatures.

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

134 mRNA levels of inflammatory mediators in P. gingivalis-infected GFs.

135 , reduces expression of Wnt3a and Dvl3 in P. gingivalis-infected gingival tissues, and increases dise

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

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

138 Compared to non-infected cells, P. gingivalis infection decreased TEER (P < 0.0001) of HGEp

139 P. gingivalis infection induced the expansion of three subp

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

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

142 uc_1100 on macrophage polarization during P. gingivalis infection were evaluated in a murine model of

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

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

145 n and mitigates the neurotoxic effects of P. gingivalis infection.

146 ve therapeutic targets for the control of P. gingivalis infections.

147 Evidence of P. gingivalis infiltration has been detected in autopsy spe

148 ected with P. gingivalis show evidence of P. gingivalis infiltration, along with various neuropatholo

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

150 In contrast, P. gingivalis internalization and intracellular survival in

151 has no effect on association and entry of P. gingivalis into human oral keratinocytes.

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

153 am-negative bacterial pathogen Porphyromonas gingivalis is a key event in the initiation and developm

154 Porphyromonas gingivalis is a keystone pathogen of periodontitis.

155 Porphyromonas gingivalis is a keystone pathogen that contributes to pe

156 Porphyromonas gingivalis is a keystone pathogen, and its Lys-gingipain

157 Porphyromonas gingivalis is a member of the dysbiotic oral microbiome

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

159 Porphyromonas gingivalis is a periodontal pathogen implicated in a ran

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

161 Overabundance of Porphyromonas gingivalis is associated with shorter survival of ESCC p

162 rking hypothesis that synthesis of SLs by P. gingivalis is central to its ability to manipulate the h

163 Porphyromonas gingivalis is considered a keystone pathogen in the dise

164 Porphyromonas gingivalis is considered a keystone pathogen that contri

165 Porphyromonas gingivalis is strongly implicated in periodontal inflamm

166 The Gram-negative anaerobe, Porphyromonas gingivalis, is a key periodontal pathogen, and several l

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

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

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

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

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

172 5 IU/mL exhibited five-fold more abundant P. gingivalis levels than patients below the threshold.

173 Porphyromonas gingivalis, like other bacteria belonging to the phylum

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

175 7BL/6J mice were cultured with Porphyromonas gingivalis lipopolysaccharide (LPS) and cytosine-phospho

176 ammatory gene expression using Porphyromonas gingivalis lipopolysaccharide (LPS) as a pathogen, 2) a

177 ipopolysaccharide (Ec-LPS) and Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) stimulation, usin

178 sence of ultrapure or standard Porphyromonas gingivalis lipopolysaccharide (PgLPS), Pam3CSK4, or inte

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

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

181 In our PDL progenitor cell culture model, P. gingivalis LPS increased H3K4me3 histone methylation on

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

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

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

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

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

187 on by the periodontal pathogen Porphyromonas gingivalis may link these two inflammatory and degenerat

188 show, for the first time, that OMVs from P. gingivalis mediate increased vascular permeability, lead

189 We recently demonstrated P. gingivalis-mediated gut barrier breakdown and exacerbati

190 oreover, deletion of PPAD did not prevent P. gingivalis-mediated intestinal barrier breakdown and exa

191 In addition, using an in vivo P. gingivalis-mediated periodontal disease model, we show t

192 (BMM) and THP-1 cells were infected with P. gingivalis (MOI = 20:1) and a panel of cytokines were me

193 hough the periodontal pathogen Porphyromonas gingivalis must withstand high levels of nitrosative str

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

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

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

197 efore, this study assessed the effects of P. gingivalis OMVs on the endothelium.

198 both groups at 3 and 6 months, Porphyromonas gingivalis only in the test group.

199 Targeting P. gingivalis or its activated effectors may provide novel

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

201 ed even more pronounced, by six-fold more P. gingivalis (P = 0.025), in patients with a DAS-28 score

202 nthesized and their effects on Porphyromonas gingivalis (P. gingivalis) elicited inflammation were ev

203 sythia (T.f.), 2.5 x 10(4) for Porphyromonas gingivalis (P.g.), 5.3 x 10(3) for Prevotella intermedia

204 tant role of PDLSCs in the recognition of P. gingivalis, paracrine recruitment and activation of anti

205 of ACPA through the activity of a unique P. gingivalis peptidylarginine deiminase (PPAD) produced by

206 acrophages exposed to LPS from Porphyromonas gingivalis (Pg LPS).

207 dy, we sought to explore the virulence of P. gingivalis (Pg) affecting glycogen synthase kinase 3 bet

208 Porphyromonas gingivalis (Pg) capsule enables evasion from phagocytosi

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

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

211 ion of a periodontal pathogen, Porphyromonas gingivalis (Pg) to WT mice results in insulin resistance

212 on of the periodontal pathogen Porphyromonas gingivalis (Pg) with commensal streptococci promotes Pg

213 of Tannerella forsythia (Tf), Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (

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

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

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

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

218 gated the role of GRHL2 in the Porphyromonas gingivalis (Pg)-induced impairment of epithelial barrier

219 We documented earlier that Porphyromonas gingivalis(Pg), keystone oral-pathobiont, causative of P

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

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

222 is and the anaerobic bacterium Porphyromonas gingivalis plays a key role in driving chronic inflammat

223 se data demonstrate that encapsulation of P. gingivalis plays a key role in the alveolar bone resorpt

224 Intracellular invasion of P. gingivalis potentiated proliferation, migration, invasio

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

226 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia,

227 is investigation was to determine whether P. gingivalis produces additional lipid classes similar to

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

229 Gingipains, a class of P. gingivalis proteases, are found in association with neur

230 dy activity specific to autocitrullinated P. gingivalis proteins.

231 whether autocitrullinated proteins in the P. gingivalis proteome serve as cross-activation targets in

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 appears to be the primary means by which P. gingivalis responds to NO(2) (-)-based stress.

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

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

240 P. gingivalis secretes proteolytic gingipains (Kgp and RgpA

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

242 The brains of mice orally infected with P. gingivalis show evidence of P. gingivalis infiltration,

243 P. gingivalis signature genes based on its activated effect

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

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

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

247 oduction of pro-inflammatory cytokines in P. gingivalis-stimulated innate immune cells.

248 so observed following LPS from Porphyromonas gingivalis stimulation during osteogenic differentiation

249 The Porphyromonas gingivalis strain ATCC 33277 (33277) and 381 genomes are

250 immune responses to these highly related P. gingivalis strains.

251 xpression profile induced by TNFalpha and P. gingivalis, suggesting a critical role for HDAC3 in GF i

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

253 These results demonstrate that P. gingivalis synthesizes glycine lipids and that these lip

254 hich included all Socransky red bacteria (P. gingivalis, T. forsythia, T. denticola).

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

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

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

258 ted to determine the levels of Porphyromonas gingivalis, Tannerella forsythia, and Fusobacterium nucl

259 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Fusobacterium nucl

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

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

262 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia,

263 ibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, F

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

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

266 erine-glycine lipids are also produced by P. gingivalis The goal of this investigation was to determi

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

268 Fim fimbriae, which are also expressed by P. gingivalis These results support a donor strand-based as

269 nd two isogenic non-capsulated mutants of P. gingivalis, this study aimed to analyze whether P. gingi

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

271 pathobiotic bacteria, such as Porphyromonas gingivalis, through small danger molecule signaling.

272 microbiome that influence the ability of P. gingivalis to colonize the placenta may drive differenti

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

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

275 tion promoted the tolerance of Porphyromonas gingivalis to oxidative stress under micro-aerobic condi

276 e lipids) affords a mechanism that allows P. gingivalis to persist in homeostasis with its host.

277 ontitis model, we assessed the ability of P. gingivalis to produce ISAR and FGR in Sprague Dawley (SD

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

279 d for 24 h and challenged with Porphyromonas gingivalis total protein extract (PgPE) (0 or 2 ug/mL) f

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

281 red complex pathogens, namely, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythi

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

283 thogens Prevotella intermedia, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, a

284 P. gingivalis utilizes protease-generated peptides derived

285 nd 1 minute, reducing, mainly, Porphyromonas gingivalis viability, with 2.78 and 1.7 log(10) CFU mL(-

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

287 Using a novel P. gingivalis W50 PPAD mutant strain, incapable of protein

288 Porphyromonas gingivalis W83 biofilm was cultured on titanium discs an

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

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

291 direct physical contact between fungi and P. gingivalis was initiated via a modulation of gene expres

292 Of the three species, P. gingivalis was reduced in both reservoirs 4-6 wk after t

293 of Streptococcus sanguinis and Porphyromonas gingivalis was significantly reduced in the PDLLA-AMX gr

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

295 or non-encapsulated ATCC 33277 strains of P. gingivalis were used as controls.

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

297 mvastatin, being highly effective against P. gingivalis while not affecting commensal microbiota, pos

298 d fimbriae (pili) mediate interactions of P. gingivalis with other bacteria and with host cells throu

299 We show that treatment of P. gingivalis with peptides corresponding to the conserved

300 that a protective environment existed for P. gingivalis within developed fungal biofilm formed under