ライフサイエンスコーパス: P. gingivalis

1 P. gingivalis colonization of the periodontal pockets ma

2 P. gingivalis did not increase Wnt3a mRNA levels, a find

3 P. gingivalis DPP5 was composed of 684 amino acids with

4 P. gingivalis exhibited more straightforward association

5 P. gingivalis IgG1 and IgG2 were analyzed.

6 P. gingivalis induced a significant (p < 0.01) increase

7 P. gingivalis induced the rapid production of ROS, which

8 P. gingivalis infection induced the expansion of three s

9 P. gingivalis is found on and within oral and gingival e

10 P. gingivalis LPS and AGE in combination caused signific

11 P. gingivalis LPS preparations also increased IL-10 and

12 P. gingivalis LPS preparations increased IFN-gamma level

13 P. gingivalis porU and porV have also been linked to T9S

14 P. gingivalis secretes proteolytic gingipains (Kgp and R

15 P. gingivalis sonicated extract, P. gingivalis lipopolys

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

17 P. gingivalis, P. intermedia, T. forsythia, and T. denti

18 P. gingivalis-induced TLR2 expression in HGFs is partial

19 P. gingivalis-infected WT mice exhibited significantly i

20 P. gingivalis-LPS induced the secretion of interleukin (

21 P. gingivalis-NDK during infection inhibits extracellula

22 unts of A. actinomycetemcomitans (P <0.001), P. gingivalis (P = 0.042), and T. forsythia (P <0.001) w

23 cetemcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. dentico

24 n HeLa and TERT-2 cells exposed to the HIV-1-P. gingivalis complexes 2 hr after the initial infection

25 Significantly more (11.8%) P. gingivalis attached to the cp-Ti disks than to the Ti

26 onsecutive days (days 0 to 3) with 1 x 10(9) P. gingivalis bacteria (strain ATCC 33277).

27 2X7 receptor expression was upregulated in a P. gingivalis oral infection model, and reduced IFN-gamm

28 rfere with the initiation and formation of a P. gingivalis-induced pathogenic community.

29 odontal pathogens (A. actinomycetemcomitans, P. gingivalis, T. forsythia, or C. rectus) were detected

30 oclasts and increased RANKL expression after P. gingivalis infection.

31 actate dehydrogenase release was found after P. gingivalis stimulation.

32 Twelve hours after P. gingivalis stimulation, NZO osteoblasts showed signif

33 not L6-Fc, into rat gingival papillae after P. gingivalis infection resulted in significantly reduce

34 significant association between IgG against P. gingivalis and ACPAs in pre-RA and markers of RA acti

35 uced both salivary IgA and serum IgG against P. gingivalis.

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

37 Smoking alters the humoral response against P. gingivalis and may increase P. gingivalis infectivity

38 proliferation elicited by TT (p < 0.001) and P. gingivalis (p < 0.001).

39 duced by LPS (p < 0.001), TG (p < 0.05), and P. gingivalis (p < 0.001), and of IL-6 in LPS- and P. gi

40 duced by LPS (p < 0.001), TG (p < 0.05), and P. gingivalis (p < 0.01), and reduced the production of

41 A. actinomycetemcomitans and P. gingivalis quantities in saliva were strongly associa

42 s was performed with combinations of AGE and P. gingivalis LPS.

43 ction of epithelial cells with F. alocis and P. gingivalis strains showed approximately 20% to 30% mo

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

45 tionship between Streptococcus cristatus and P. gingivalis, and identified arginine deiminase (ArcA)

46 infection-induced eATP release in GECs, and P. gingivalis-NDK impacts this pathway.

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

48 givalis (p < 0.001), and of IL-6 in LPS- and P. gingivalis-stimulated cultures (p < 0.001).

49 Although a trend for higher F. nucleatum and P. gingivalis concentrations in aCCP-positive patients w

50 ) between the number of cells in S phase and P. gingivalis invasion, the organism was more highly ass

51 nt correlation between surface roughness and P. gingivalis attachment.

52 C biofilm results, adherent S. sanguinis and P. gingivalis were incubated anaerobically in medium sup

53 ited the growth of adherent S. sanguinis and P. gingivalis, whereas lower concentrations resulted in

54 ion of information on age, sex, smoking, and P. gingivalis results provided an area under the curve o

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

56 alveolar bone loss, with a reduction in anti-P. gingivalis serum antibody titers compared with wild-t

57 All mucosal vaccination modes induced anti-P. gingivalis salivary IgA but not anti-P. gingivalis se

58 e-linked immunosorbent assay to measure anti-P. gingivalis IgA levels was established.

59 anti-P. gingivalis salivary IgA but not anti-P. gingivalis serum IgG.

60 monstrated alveolar bone loss and serum anti-P. gingivalis antibody titers equivalent to wild-type in

61 achment and enhanced exfoliation of attached P. gingivalis but had no influences on F. nucleatum bact

62 After 6 hours, the disks with attached P. gingivalis were stained with crystal violet, and atta

63 Direct contact between P. gingivalis and epithelial cells was not required for

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

65 demonstrate that direct interaction between P. gingivalis and S. cristatus is necessary for the cell

66 Both P. gingivalis and P. nigrescens skewed the CII-specific

67 GF-beta levels in both CP and NP groups, but P. gingivalis LPS1690 showed a three-fold increase on IL

68 ytes and macrophages but was not affected by P. gingivalis.

69 activation of the uPA proteolytic cascade by P. gingivalis being required for the pathogen to induce

70 ta-Catenin activation in epithelial cells by P. gingivalis may contribute to a proliferative phenotyp

71 The stimulatory effects by P. gingivalis-LPS were more evident when cells were cult

72 rding the subpopulations of MDSC expanded by P. gingivalis infection.

73 truction of crestal alveolar bone induced by P. gingivalis colonization occurred regardless of the pr

74 Thus, the inflammatory response induced by P. gingivalis infection promotes the expansion of immune

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

76 -miR-2137 to control inflammation induced by P. gingivalis infection.

77 experimental periodontitis model induced by P. gingivalis-soaked ligatures.

78 biofilm formation and host cell invasion by P. gingivalis by controlling the expression and biosynth

79 invasion of the aortic adventitial layer by P. gingivalis.

80 3beta were also proteolytically processed by P. gingivalis gingipains.

81 d extracellular polysaccharide production by P. gingivalis.

82 induced IL-1beta processing and secretion by P. gingivalis-infected macrophages.

83 th outer membrane vesicles naturally shed by P. gingivalis, we observed generation of C5a totally cit

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

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

86 In conclusion, P. gingivalis infection induced infiltration of function

87 Conversely, P. gingivalis infection-induced alveolar bone loss was a

88 d that this can be detected by the different P. gingivalis LPS structures.

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

90 opment in mice infected with PPAD-expressing P. gingivalis, our findings support a crucial role of PP

91 P. gingivalis sonicated extract, P. gingivalis lipopolysaccharide, P. gingivalis DNA, and

92 es produced more A20 than WT cells following P. gingivalis challenge.

93 vivo abrogated alveolar bone loss following P. gingivalis infection.

94 ion of beta-catenin in the nucleus following P. gingivalis infection was confirmed by immunofluoresce

95 e of suture, have antimicrobial activity for P. gingivalis and E. faecalis.

96 resents an important pathogenesis factor for P. gingivalis.

97 -mediated activation of JAK2 is required for P. gingivalis-induced inflammatory cytokine production a

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

99 the present study, we identified the fourth P. gingivalis enzyme, DPP5.

100 lly, although the secretion of IL-1beta from P. gingivalis-infected macrophages was dependent on NLRP

101 nvestigate how lipopolysaccharide (LPS) from P. gingivalis stimulates bone resorption.

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

103 ucture of the CTD of gingipain B (RgpB) from P. gingivalis, alone and together with a preceding immun

104 prove the health of millions who suffer from P. gingivalis-mediated periodontal disease.

105 ured GECs or green-fluorescent-protein (GFP)-P. gingivalis-NDK transfected GECs revealed a perinuclea

106 ency in myeloid cells also promotes a higher P. gingivalis lipopolysaccharide-induced inflammatory re

107 chronic in vitro infection model to test if P. gingivalis can induce DNA methylation in normal gingi

108 In P. gingivalis-administered mice blood endotoxin levels t

109 In P. gingivalis-infected BMMs, mmu-miR-155-5p significantl

110 re detected at day 7 and peaked at day 28 in P. gingivalis-infected rats.

111 chondrial dehydrogenase activity but also in P. gingivalis-LPS-induced production of IL-6, TNF-alpha,

112 Whether this change in P. gingivalis levels leads to biofilm alteration with re

113 the benefit appears to stem from changes in P. gingivalis levels in the DHA + aspirin treatment grou

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

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

116 No significant difference in P. gingivalis attachment was noted among the corroded gr

117 Bacteroidales was significantly elevated in P. gingivalis-administered mice which coincided with inc

118 lectively alter virulence gene expression in P. gingivalis, and PGN_0294 and PGN_0806 may serve as re

119 econd messenger has not been investigated in P. gingivalis, mainly due to a lack of an annotation reg

120 ffect on the intracellular c-di-GMP level in P. gingivalis.

121 tress resistance and virulence regulation in P. gingivalis.

122 t the PG_2212 gene was highly upregulated in P. gingivalis under conditions of prolonged oxidative st

123 ponse against P. gingivalis and may increase P. gingivalis infectivity, strengthening the evidence th

124 ity in aged mice may contribute to increased P. gingivalis colonization following inoculation and inc

125 ression and production of several well-known P. gingivalis virulence factors including fimbrial prote

126 ated with fluorescein isothiocyanate-labeled P. gingivalis, and phagocytosis was measured in a fluoro

127 de tissues and significantly (p < 0.01) less P. gingivalis-induced bone resorption compared with cont

128 d extract, P. gingivalis lipopolysaccharide, P. gingivalis DNA, and tumor necrosis factor-alpha(TNF-a

129 led wild-type Porphyromonas gingivalis, live P. gingivalis protease-deficient mutant KDP128, and live

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

131 LPS P. gingivalis and Pam2 also up-regulated RANKL and osteo

132 LPS P. gingivalis and Pam2 robustly enhanced osteoclast form

133 LPS P. gingivalis stimulated mineral release and matrix degr

134 LPS P. gingivalis stimulated RANKL in parietal osteoblasts d

135 The effects by LPS P. gingivalis and four other TLR2 ligands on bone resorp

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

137 uted to TNF production in naive macrophages, P. gingivalis preferentially exploited TLR2 in endotoxin

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

139 The isogenic mutant P. gingivalis FLL366 (DeltaPG_2212) showed increased sen

140 Now we show that in neutrophils P. gingivalis disarms a host-protective TLR2-MyD88 pathw

141 The ability of P. gingivalis to activate cells via TLR2 or TLR4 was con

142 lly, SAPP was able to impinge the ability of P. gingivalis to dysregulate innate immunity by repressi

143 TLR2-deficient mice restored the ability of P. gingivalis to induce alveolar bone loss in vivo.

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

145 of the extracellular proteolytic activity of P. gingivalis at the site of infection.

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

147 highly effective in inhibiting adherence of P. gingivalis to host cells.

148 2) plays a critical role in the adherence of P. gingivalis to host cells.

149 kers showed significantly greater amounts of P. gingivalis, A. actinomycetemcomitans, and T. forsythi

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

151 -spectrometry method revealed association of P. gingivalis-NDK to the myosin-9 motor molecule.

152 on the adhesive and invasive capabilities of P. gingivalis, which are required for its pathogenicity.

153 pletion led to greatly improved clearance of P. gingivalis.

154 nfocal microscopy indicate colocalization of P. gingivalis with TG2 on the surface of HEp-2 epithelia

155 were treated with various concentrations of P. gingivalis-LPS under normal (5.5 mM) or high (25 mM)

156 Resolvin D1 altered the cytotoxicity of P. gingivalis supernatant on HGFs.

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

158 ly, we find that in vivo clonal expansion of P. gingivalis-specific Th cells and induced regulatory T

159 t growth rate was not altered by exposure of P. gingivalis to SAPP, while monospecies and heterotypic

160 smoking is known to alter the expression of P. gingivalis surface components and compromise immunogl

161 partner species that enhances the fitness of P. gingivalis while diminishing its virulence.

162 PDT protocol presented inferior frequency of P. gingivalis at 3 months when compared with the other t

163 Bypassing LCs with systemic immunization of P. gingivalis resulted in a predominantly P. gingivalis-

164 as for caspase 1 activation irrespective of P. gingivalis fimbriae.

165 gates the effects of two lipid A isoforms of P. gingivalis, lipopolysaccharide (LPS)1435/1449 and LPS

166 f A. actinomycetemcomitans or serotype K1 of P. gingivalis, higher levels of TLR2 or TLR4, respective

167 of P. gingivalis infection, and the level of P. gingivalis infection was significantly correlated wit

168 d in a significant reduction in the level of P. gingivalis infection, and the level of P. gingivalis

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

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

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

172 young mice was linked to enhanced levels of P. gingivalis and reduced bacterial diversity.

173 linical periodontal parameters and levels of P. gingivalis, T. denticola, and T. forsythia, but not A

174 Specific serine-containing lipids of P. gingivalis, called lipid 654 and lipid 430, were iden

175 t could be exploited for the manipulation of P. gingivalis levels in oral communities and preventing

176 red for the peptide-fermenting metabolism of P. gingivalis.

177 Ultrastructural and confocal microscopy of P. gingivalis-co-cultured GECs or green-fluorescent-prot

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

179 esults, using conditional fimbria mutants of P. gingivalis, show that P. gingivalis infection of MoDC

180 ere positively correlated with the number of P. gingivalis in subgingival plaque.

181 uch and increases neutrophil phagocytosis of P. gingivalis in the transgenic animals; cutaneous fat d

182 vE1 increased the neutrophil phagocytosis of P. gingivalis in WT animals but had no impact in db/db a

183 ether, the results indicate the potential of P. gingivalis to disrupt the control system of KLKs, pro

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

185 ew insight into the biological properties of P. gingivalis LPS lipid A moiety that could critically m

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

187 loss may be on the arg-gingipain protease of P. gingivalis.

188 Two surface proteins of P. gingivalis, PGN_0294 and PGN_0806, were found to inte

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

190 A increased the colonization and survival of P. gingivalis in a murine oral infection model.

191 ptosome and XIAP as intracellular targets of P. gingivalis, contributing to the deterioration of peri

192 IL-33 treatment of P. gingivalis-infected mice significantly exacerbated al

193 contributes further to our understanding of P. gingivalis-induced modulation of miRNAs and their phy

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

195 t a crucial role of PPAD in the virulence of P. gingivalis.

196 DC-SIGN on MoDCs and minor mfa-1 fimbriae on P. gingivalis and is evidenced by robust upregulation of

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

198 Here we identify gingipains as the only P. gingivalis proteases responsible for SPINK6 degradati

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

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

201 ) with different A. actinomycetemcomitans or P. gingivalis serotypes in the presence or absence of an

202 regardless of the presence of mucosal LCs or P. gingivalis-specific Th17 cells.

203 compared to that in sham-infected WT mice or P. gingivalis-infected TLR9(-/-) mice, which were resist

204 Key pathogens P. gingivalis, T. forsythia, T. denticola, P. micra, C.

205 us mitis biofilm when the periodontopathogen P. gingivalis is present.

206 ablished in vitro tobacco-induced phenotypic P. gingivalis changes would be reflected in vivo.

207 sion between mice treated with ligation plus P. gingivalis infection and mice treated with ligation a

208 nd Tlr4(-/-) mice treated with ligation plus P. gingivalis infection showed significantly increased b

209 ce, bone resorption induced by ligation plus P. gingivalis infection was antagonized by local anti-RA

210 of P. gingivalis resulted in a predominantly P. gingivalis-specific Th1 response regardless of whethe

211 rains and their respective LPS preparations, P. gingivalis wild type, but not the lipid A mutants, ha

212 CX3CR1(hi) monocyte/macrophages promote P. gingivalis survival by downregulating neutrophil phag

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

214 Macrophage depletion reduced P. gingivalis infection and alveolar bone resorption by

215 As previously reported, P. gingivalis remodels the oral microbiota into a dysbio

216 The combination of saliva P. gingivalis quantity with pathogen-specific host respo

217 eptide array analysis, we identified several P. gingivalis-binding sites of ArcA, which led to the di

218 ors examined the humoral response to several P. gingivalis strains as well as specific tobacco-regula

219 ed the effect of JAK2 inhibition to suppress P. gingivalis-induced IL-6 and IL-1beta levels.

220 Overall, we conclude that P. gingivalis actively "commandeers" DCs by reprogrammin

221 The present data demonstrate that P. gingivalis downregulates proliferation and promotes a

222 cript, we present results demonstrating that P. gingivalis induces S. mitis death and DNA fragmentati

223 mokine receptor knockout mice and found that P. gingivalis clearance is significantly improved in the

224 In this study, we found that P. gingivalis did not induce the expression of the T-cel

225 Based on these results, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown

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

227 istent with previous reports indicating that P. gingivalis invasion of cells is mediated by alpha5 in

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

229 fimbria mutants of P. gingivalis, show that P. gingivalis infection of MoDCs induces an angiogenic m

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

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

232 Previous studies have shown that P. gingivalis accelerates the cell cycle and prevents ap

233 Our findings suggest that P. gingivalis HmuY may be associated with increased IL-6

234 This study suggests that P. gingivalis exacerbates ligature-induced, RANKL-depend

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

236 K1, and AKT were selectively degraded by the P. gingivalis lysine-specific gingipain (Kgp) in human e

237 were significantly elevated at day 28 in the P. gingivalis-infected group compared to levels in the u

238 d, confirming the requirement of TLR2 in the P. gingivalis-mediated inflammatory response.

239 e of a novel polymerization mechanism of the P. gingivalis fimbriae.

240 ely correlated with invasive activity of the P. gingivalis strains tested, even when the binding affi

241 In both mouse strains, the P. gingivalis-specific IgG Ab subclass and serum cytokin

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

243 nction had greater production of antibody to P. gingivalis, greater IL-12 expression, and more plasma

244 ese data reveal a multidimensional aspect to P. gingivalis-S. gordonii interactions and establish pAB

245 ytokine response of oral epithelial cells to P. gingivalis.

246 n in the NP group (P <0.05) when compared to P. gingivalis LPS1435/144.

247 verged in that P. nigrescens, in contrast to P. gingivalis, suppressed the joint-protective type 2 cy

248 e of elevated PA or OA levels and exposed to P. gingivalis.

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

250 ly expressed in dysfunctional cells prior to P. gingivalis stimulation, the cytokine expression was i

251 th CP may differ in the cytokine response to P. gingivalis but not E. coli LPS.

252 showed an augmented inflammatory response to P. gingivalis in the presence of hyperlipidemic PA level

253 pe of the gingival infiltrate in response to P. gingivalis infection.

254 ) and increased in all groups in response to P. gingivalis inoculation (P < 0.01), whereas bone remod

255 evaluate whether the overall IgG response to P. gingivalis is suppressed in smokers in vivo and wheth

256 OECs have a unique response to P. gingivalis LPS, where miR146a and miR155 play a regul

257 tokine production in WT cells in response to P. gingivalis, thereby implicating TLR9 in inflammatory

258 of proinflammatory cytokines in response to P. gingivalis.

259 -1 family cytokine IL-36gamma in response to P. gingivalis.

260 T cell proliferation (P < 0.05) responses to P. gingivalis were detected at day 7 and peaked at day 2

261 ng differentiation of Th17 cells specific to P. gingivalis.

262 ginine deiminase (PPAD), an enzyme unique to P. gingivalis among bacteria, which converts Arg residue

263 ing lymph nodes were higher in IL-33-treated P. gingivalis-infected mice versus phosphate buffered sa

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

265 We examined two P. gingivalis lipid A phosphatase mutants which contain

266 xpressing diminished cytokine signaling upon P. gingivalis stimulation.

267 Here, we utilize P. gingivalis mutant strains to show that pathogen-diffe

268 y inhibited the toxic effects of 13.5% (v/v) P. gingivalis supernatant on HGFs (P = 0.002).

269 <0.05) but not laboratory (ATCC 33277, W83) P. gingivalis strains.

270 eal a new host-pathogen interaction in which P. gingivalis activates a critical host proteolytic path

271 effect was observed in fibroblasts in which P. gingivalis increased cell death and apoptosis.

272 cristatus as the signaling molecule to which P. gingivalis responds by repressing the expression and

273 re found to be higher in individuals in whom P. gingivalis was detected than for those without P. gin

274 Infection of gingival epithelial cells with P. gingivalis did not influence the phosphorylation stat

275 ic treatment of normal epithelial cells with P. gingivalis introduced de novo DNA methylation within

276 in the oral cavity following challenge with P. gingivalis Our findings provide an explanation for ba

277 n oral epithelial cells were challenged with P. gingivalis.

278 xpressed more proteins during coculture with P. gingivalis W83 than with P. gingivalis 33277.

279 fected SOCS-3-knockout mice as compared with P. gingivalis-infected WT mice by direct morphologic mea

280 Wnt3a mRNA levels, a finding consistent with P. gingivalis-induced proteolytic processing causing the

281 es (WBCCs) were stimulated for 48 hours with P. gingivalis LPS1435/1449 and LPS1690 and Escherichia c

282 row and spleen cells from mice infected with P. gingivalis and controls for surface expression of CD1

283 -engrafted Kit(W-sh/W-sh) mice infected with P. gingivalis demonstrated alveolar bone loss and serum

284 bserved in the gingiva of mice infected with P. gingivalis in a periodontitis oral gavage model.

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

286 olar bone loss following oral infection with P. gingivalis, and thus establish a central role for TNF

287 in determining the outcome of infection with P. gingivalis.

288 Disks were inoculated with P. gingivalis and incubated anaerobically at 37 degrees

289 Strategies that interfere with P. gingivalis colonization and expression of virulence f

290 PRP interfered with P. gingivalis and A. actinomycetemcomitans attachment an

291 g at week 10, mice were infected orally with P. gingivalis (W50) or placebo to induce alveolar bone l

292 LF from the same donors were stimulated with P. gingivalis LPS or with two synthetic ligands of TLR2,

293 control C57BL/6J mice, were stimulated with P. gingivalis.

294 to be infected orally and systemically with P. gingivalis (P <0.001), as determined by 16S RNA analy

295 g coculture with P. gingivalis W83 than with P. gingivalis 33277.

296 s CpG compared to those in mice treated with P. gingivalis LPS or CpG alone.

297 TGF)-beta1 (P = 0.07) from HGFs treated with P. gingivalis supernatant.

298 significantly increased with treatment with P. gingivalis LPS plus CpG compared to those in mice tre

299 h or without resolvin D1 and with or without P. gingivalis supernatant.

300 ngivalis was detected than for those without P. gingivalis (P <0.01).