ライフサイエンスコーパス: A. actinomycetemcomitans

1 A. actinomycetemcomitans activates the p38 mitogen-activ

2 A. actinomycetemcomitans and AL were frequently found in

3 A. actinomycetemcomitans and P. gingivalis quantities in

4 A. actinomycetemcomitans and Staphylococcus species do n

5 A. actinomycetemcomitans binding to SHA was irreversible

6 A. actinomycetemcomitans can also cause systemic disease

7 A. actinomycetemcomitans cells rapidly lost viability at

8 A. actinomycetemcomitans cells were highly sensitive to

9 A. actinomycetemcomitans IHFalpha and IHFbeta were expre

10 A. actinomycetemcomitans is a slow-growing bacterium tha

11 A. actinomycetemcomitans LPS induced severe bone loss ov

12 A. actinomycetemcomitans migrated from BECs to HA in viv

13 A. actinomycetemcomitans preferentially colonized the EC

14 A. actinomycetemcomitans produces leukotoxin (LtxA), whi

15 A. actinomycetemcomitans secretes a protein toxin, leuko

16 A. actinomycetemcomitans serotype did not appear to infl

17 A. actinomycetemcomitans serotypes a, b, and c were equa

18 A. actinomycetemcomitans strains can produce high or low

19 A. actinomycetemcomitans strains expressing EmaA with th

20 A. actinomycetemcomitans was detected by polymerase chai

21 A. actinomycetemcomitans was significantly associated wi

22 A. actinomycetemcomitans, P. gingivalis, T. forsythia, P

23 nts harbored P. gingivalis (43%; P < 0.001); A. actinomycetemcomitans, (31%; P = 0.025), or T. forsyt

24 Illumina MiSeq platform was performed for 31 A. actinomycetemcomitans and 2 A. aphrophilus strains.

25 Eight of 38 A. actinomycetemcomitans-positive and none of 58 A. acti

26 established that included a test group of 38 A. actinomycetemcomitans-positive students (36 periodont

27 ctinomycetemcomitans-positive and none of 58 A. actinomycetemcomitans-negative students showed bone l

28 one A. actinomycetemcomitans-negative and 63 A. actinomycetemcomitans-positive periodontally healthy

29 We identified 691 A. actinomycetemcomitans transcriptional start sites and

30 aae apiA double mutant completely abrogated A. actinomycetemcomitans binding to both human and Old W

31 Streptococcus, Actinomyces, A. actinomycetemcomitans, and total anaerobic counts wer

32 k2(-/-) mice compared to Mk2(+/+) mice after A. actinomycetemcomitans treatment.

33 owed significant phagocytic activity against A. actinomycetemcomitans.

34 gocytic ability of murine mast cells against A. actinomycetemcomitans was confirmed.

35 /mL AZM or 16 mug/mL AMX (equipotent against A. actinomycetemcomitans).

36 levels of systemic immunoreactivity against A. actinomycetemcomitans Ltx are associated with decreas

37 n of murine mast cells as phagocytes against A. actinomycetemcomitans, mainly in the absence of opson

38 nces of Parvimonas micra, Filifactor alocis, A. actinomycetemcomitans, and Peptostreptococcus sp. hum

39 The genetic heterogeneity among A. actinomycetemcomitans strains has been long recognize

40 We report the first genome sequence of an A. actinomycetemcomitans strain isolated from an Old Wor

41 ng from the separation of A. aphrophilus and A. actinomycetemcomitans through gain and loss of genes

42 core genes distinguished A. aphrophilus and A. actinomycetemcomitans.

43 functionally active in Escherichia coli and A. actinomycetemcomitans using truncated PhoA and Aae ch

44 PRP interfered with P. gingivalis and A. actinomycetemcomitans attachment and enhanced exfolia

45 tive antibodies induced by P. gingivalis and A. actinomycetemcomitans include anti-phosphorylcholine

46 nterestingly, in flow cells F. nucleatum and A. actinomycetemcomitans exhibited mutualism, and, altho

47 mitans outer membrane protein 29 (Omp29) and A. actinomycetemcomitans lipopolysaccharide (LPS) were i

48 nomycetemcomitans but not with S. oralis and A. actinomycetemcomitans.

49 P. gingivalis grew with Veillonella sp. and A. actinomycetemcomitans but not with S. oralis and A. a

50 Being A. actinomycetemcomitans-positive or -negative did not c

51 d V. harveyi bioluminescence induced by both A. actinomycetemcomitans AI-2 and V. harveyi AI-2 in a d

52 ts for treating chronic infections caused by A. actinomycetemcomitans and other PGA-producing bacteri

53 Biofilm formation by A. actinomycetemcomitans was virtually eliminated upon i

54 us is required for optimal biofilm growth by A. actinomycetemcomitans.

55 I-2 itself is required for biofilm growth by A. actinomycetemcomitans.

56 us is required for optimal biofilm growth by A. actinomycetemcomitans.

57 PMNs cope with an overwhelming infection by A. actinomycetemcomitans.

58 treptococcal metabolite hydrogen peroxide by A. actinomycetemcomitans, which stimulates a genetic pro

59 O2 at a low concentration range regulated by A. actinomycetemcomitans enhanced the biofilm formation.

60 .2% of students had LAP, while 13.7% carried A. actinomycetemcomitans, including 16.7% of African-Ame

61 The majority of the individuals carrying A. actinomycetemcomitans (80.1%) (P <0.001) and of the p

62 e that NADPH oxidase is important to control A. actinomycetemcomitans infection in the murine oral ca

63 d the rate by which intact bacteria depleted A. actinomycetemcomitans AI-2 from solution.

64 e to express rbsB was deficient in depleting A. actinomycetemcomitans AI-2 from solution relative to

65 associated with increased odds of detecting A. actinomycetemcomitans, P. gingivalis, and T. forsythe

66 y of infection (MOI) of 10(2) with different A. actinomycetemcomitans or P. gingivalis serotypes in t

67 s study is to evaluate the role of LF during A. actinomycetemcomitans-induced periodontitis.

68 MK2 signaling in chemokine regulation during A. actinomycetemcomitans pathogenesis.

69 to regulation of chemokine signaling during A. actinomycetemcomitans-induced inflammation and bone l

70 the following factors (interaction effect): A. actinomycetemcomitans-positive or -negative at baseli

71 i AI-2 receptor (LuxP) with AI-2 from either A. actinomycetemcomitans or V. harveyi.

72 In this environment, A. actinomycetemcomitans faces numerous host- and microb

73 00 (also known as ApiA), a surface-expressed A. actinomycetemcomitans adhesin, is that second adhesin

74 t rats received injections of formalin-fixed A. actinomycetemcomitans into the gingival papillae, and

75 n response to pretreatment of GEC with fixed A. actinomycetemcomitans and IFN-gamma.

76 rial levels and prediabetes were as follows: A. actinomycetemcomitans, 2.48 (1.34, 4.58), P = 0.004;

77 developed one colony forming unit (CFU) for A. actinomycetemcomitans, whereas zero of 10 samples dev

78 3, respectively, developed multiple CFUs for A. actinomycetemcomitans and P. gingivalis.

79 Samples were taken from each child for A. actinomycetemcomitans.

80 ability to grow in biofilms is essential for A. actinomycetemcomitans virulence, strains that were de

81 .01) counts of all target species except for A. actinomycetemcomitans.

82 RbsB competed more effectively with LuxP for A. actinomycetemcomitans AI-2.

83 gingivalis and approximately 2.0 microM for A. actinomycetemcomitans (N = five experiments each).

84 ween the groups were seen after 3 months for A. actinomycetemcomitans and P. gingivalis, and after 12

85 ns and 41 participants who were negative for A. actinomycetemcomitans.

86 luding 41 participants who were positive for A. actinomycetemcomitans and 41 participants who were ne

87 Patients who were positive for A. actinomycetemcomitans had no specific benefit from am

88 One patient was positive for A. actinomycetemcomitans in the three types of samples.

89 sis is to determine if patients positive for A. actinomycetemcomitans with moderate to advanced perio

90 occurred with approximately 0.3 nM RbsB for A. actinomycetemcomitans AI-2 and 15 nM RbsB for V. harv

91 insight into metabolic pathways required for A. actinomycetemcomitans in vivo fitness.

92 BECs are a likely reservoir for A. actinomycetemcomitans tooth colonization.

93 Since the BEC is a prominent reservoir for A. actinomycetemcomitans, identification of this second

94 PI, GI, total bacterial load, T. forsythia, A. actinomycetemcomitans, and GCF volume.

95 timulation with partially purified AI-2 from A. actinomycetemcomitans or conditioned medium from V. h

96 We demonstrated that B cells from A. actinomycetemcomitans-immunized animals had greater l

97 On a subject level, pooled data from A. actinomycetemcomitans-positive subjects who remained

98 Cu,Zn SOD was purified from A. actinomycetemcomitans to homogeneity and remained enz

99 ection in the available flp-2 sequences from A. actinomycetemcomitans, suggesting that flp-2 does not

100 minD superfamily of genes and that TadZ from A. actinomycetemcomitans (AaTadZ) forms a polar focus in

101 f strains antagonistic toward P. gingivalis, A. actinomycetemcomitans, and F. nucleatum was found to

102 The PCR-positive triad, P. gingivalis, A. actinomycetemcomitans, and P. intermedia, was associa

103 nificantly greater amounts of P. gingivalis, A. actinomycetemcomitans, and T. forsythia than never-sm

104 incubated with whole cells of P. gingivalis, A. actinomycetemcomitans, or purified components thereof

105 While growing A. actinomycetemcomitans on several types of growth medi

106 spectively 60%, 62%, and 40% of subjects had A. actinomycetemcomitans, P. gingivalis, and both bacter

107 d 2 with periodontal pockets) and 58 healthy A. actinomycetemcomitans-negative controls.

108 recognized risk factors, adults with a high A. actinomycetemcomitans titer were less likely to have

109 ion had chronic kidney disease, 22% had high A. actinomycetemcomitans antibody titer, 24% had high P.

110 However, A. actinomycetemcomitans also possesses genes related to

111 to HA in vivo and to SHA in vitro; however, A. actinomycetemcomitans movement from teeth and SHA to

112 enase H and fumarate reductase are important A. actinomycetemcomitans fitness determinants in vivo.

113 se may be capable of phosphorylating AI-2 in A. actinomycetemcomitans.

114 ons as a direct transcriptional activator in A. actinomycetemcomitans; an mlc deletion mutant reduces

115 here that this promoter (tadp) functions in A. actinomycetemcomitans.

116 However, the insertion of the GEIs in A. actinomycetemcomitans may also cause truncation and i

117 fy and determine the distribution of GEIs in A. actinomycetemcomitans.

118 gnificance of such gain and loss of genes in A. actinomycetemcomitans remains to be determined.

119 to generate random transposon insertions in A. actinomycetemcomitans, we developed and carried out a

120 own about the regulation of the tad locus in A. actinomycetemcomitans.

121 or full activity and modification of LtxA in A. actinomycetemcomitans and that modification is import

122 To determine the function of ltxC in A. actinomycetemcomitans, we generated an ltxC mutation

123 of EmaA on the LPS biosynthetic machinery in A. actinomycetemcomitans.

124 ted mutations of each gene of this operon in A. actinomycetemcomitans strain D7S.

125 Here we show that the expression of QseBC in A. actinomycetemcomitans is induced by AI-2 and that ind

126 RbsB and LsrB function as AI-2 receptors in A. actinomycetemcomitans and that the development of A.

127 iously unreported mechanism of regulation in A. actinomycetemcomitans and lead to a more complete und

128 e plasmid (pMB78) that does not replicate in A. actinomycetemcomitans and carries a region with two i

129 Although no ncRNAs have been reported in A. actinomycetemcomitans, we propose that they are likel

130 role in the regulation of LtxA secretion in A. actinomycetemcomitans in a manner independent of gene

131 brane morphology and leukotoxin secretion in A. actinomycetemcomitans.

132 es and nine small regulatory RNAs (sRNAs) in A. actinomycetemcomitans during planktonic and biofilm g

133 At 5 weeks after infection, A. actinomycetemcomitans persisted at significantly high

134 s suggest that antibody to RANKL can inhibit A. actinomycetemcomitans-specific T cell-induced periodo

135 nosylmethionine in the absence of LuxS, into A. actinomycetemcomitans did not complement the luxS mut

136 Furthermore, an isogenic A. actinomycetemcomitans mutant that was unable to expre

137 on substrates glucose, fructose, and lactate A. actinomycetemcomitans preferentially metabolizes lact

138 o Ltx is a marker for presence of leukotoxic A. actinomycetemcomitans, a presence that may modify the

139 /+) and Mk2(-/-) mice were treated with live A. actinomycetemcomitans bacteria at the midsagittal sut

140 with altered outer membrane morphology make A. actinomycetemcomitans a model organism for examining

141 omycin-loaded PMNs killed significantly more A. actinomycetemcomitans and achieved shorter half-times

142 No A. actinomycetemcomitans-negative subjects developed BL.

143 01) or T. forsythia (63%; P = 0.043) but not A. actinomycetemcomitans (50%) compared to pretreatment

144 lis, T. denticola, and T. forsythia, but not A. actinomycetemcomitans, in subgingival plaque.

145 TN<KAN-2> drastically reduced the ability of A. actinomycetemcomitans cells to grow under iron-chelat

146 in adhesin A), that mediates the adhesion of A. actinomycetemcomitans to collagen.

147 provides a comprehensive genomic analysis of A. actinomycetemcomitans and the closely related nonpath

148 emcomitans in BL and (ii) the association of A. actinomycetemcomitans and other microbes in their rel

149 y plays a central role in autoaggregation of A. actinomycetemcomitans, which may be the primary survi

150 When DCs were stimulated with serotype b of A. actinomycetemcomitans or serotype K1 of P. gingivalis

151 ndings indicate that Aae mediates binding of A. actinomycetemcomitans to BECs from humans and Old Wor

152 piA and Aae, in concert, modulate binding of A. actinomycetemcomitans to human BECs.

153 two organisms increased the total biomass of A. actinomycetemcomitans in three-species peg biofilms.

154 When this plasmid was resident in cells of A. actinomycetemcomitans and tfoX was induced, the cells

155 a USS and cloned DNA from the chromosome of A. actinomycetemcomitans was linearized by digestion wit

156 on, or alternatively that the start codon of A. actinomycetemcomitans lsrA has been incorrectly annot

157 ed in relation to increasing colonization of A. actinomycetemcomitans (OR = 1.36 for one standard dev

158 gression models, subgingival colonization of A. actinomycetemcomitans and F. nucleatum/periodonticum

159 ntitis and/or the individual colonization of A. actinomycetemcomitans.

160 The counts of A. actinomycetemcomitans (P <0.001), P. gingivalis (P =

161 The counts of A. actinomycetemcomitans and P. gingivalis were signific

162 orphism was associated with the detection of A. actinomycetemcomitans (P = 0.009; odds ratio [OR] = 3

163 nfirmed an association with the detection of A. actinomycetemcomitans (P = 0.046).

164 ase chain reaction, and culture detection of A. actinomycetemcomitans and microcomputed tomography qu

165 38 to 9.16) and the concomitant detection of A. actinomycetemcomitans and P. gingivalis (P = 0.015; O

166 creased odds of the concomitant detection of A. actinomycetemcomitans and P. gingivalis (P = 0.042; O

167 gingival plaque samples for the detection of A. actinomycetemcomitans and P. gingivalis in each of th

168 These findings suggest that detection of A. actinomycetemcomitans in periodontally healthy childr

169 confirmatory evidence that the detection of A. actinomycetemcomitans is associated with IL-6 genetic

170 ach upregulate known biofilm determinants of A. actinomycetemcomitans to contribute to biofilm format

171 omycetemcomitans and that the development of A. actinomycetemcomitans biofilms requires AI-2.

172 The trimeric adhesin EmaA of A. actinomycetemcomitans binds to collagen and is modifi

173 Electron microscopy examinations of A. actinomycetemcomitans have identified antenna-like pr

174 An approximately 22 kb GEI of A. actinomycetemcomitans, designated AAI-1, was identifi

175 train-specific variant DNA in the genomes of A. actinomycetemcomitans was identified by polymerase ch

176 er frequency of JP2 and non-JP2 genotypes of A. actinomycetemcomitans and the presence of AL in Ghana

177 this report, we show that adherent growth of A. actinomycetemcomitans on a saliva-coated surface, but

178 expression and influences biofilm growth of A. actinomycetemcomitans, we first defined the promoters

179 stic criteria for clinical identification of A. actinomycetemcomitans and potentially related bacteri

180 This was not due to heat inactivation of A. actinomycetemcomitans AI-2 since signal activity was

181 s hypothesized to mediate the interaction of A. actinomycetemcomitans with collagen.

182 iac valves to investigate the interaction of A. actinomycetemcomitans with native collagen.

183 deletion of 530 bps in a primate isolate of A. actinomycetemcomitans, which produced leukotoxin equi

184 than AMX at enhancing phagocytic killing of A. actinomycetemcomitans by neutrophils.

185 t system for AZM that may enhance killing of A. actinomycetemcomitans.

186 associated with increased systemic levels of A. actinomycetemcomitans-specific immunoglobulins and in

187 c oxide synthase (iNOS) in a murine model of A. actinomycetemcomitans-induced periodontitis.

188 imilar to that of a LuxS-deficient mutant of A. actinomycetemcomitans that is unable to produce AI-2.

189 A surprising result was that mutants of A. actinomycetemcomitans defective for production of leu

190 role in modifying the virulence potential of A. actinomycetemcomitans.

191 d between smoking status and the presence of A. actinomycetemcomitans (P <0.001).

192 the strongest predictor of both presence of A. actinomycetemcomitans and AL.

193 data are reported concerning the presence of A. actinomycetemcomitans and attachment loss (AL) in sub

194 e strongest association with the presence of A. actinomycetemcomitans in all subjects and in the subg

195 their periodontal status and the presence of A. actinomycetemcomitans in their oral cavity.

196 The presence of A. actinomycetemcomitans was demonstrated in vascular, b

197 We conclude that detecting the presence of A. actinomycetemcomitans, S. parasanguinis, and F. aloci

198 ociation between smoking and the presence of A. actinomycetemcomitans.

199 ure of a trimeric autotransporter protein of A. actinomycetemcomitans.

200 The overall carrier rate of A. actinomycetemcomitans was 54.4%, and the highly leuko

201 g, desorption, transfer, and reattachment of A. actinomycetemcomitans wild-type and mutant strains to

202 The GEIs may increase the gene repertoire of A. actinomycetemcomitans.

203 ular components that mediate the response of A. actinomycetemcomitans to AI-2 have not been fully cha

204 that RbsB may play a role in the response of A. actinomycetemcomitans to AI-2.

205 led every 6 months to assess (i) the role of A. actinomycetemcomitans in BL and (ii) the association

206 Analysis of the complete genome sequence of A. actinomycetemcomitans (www.oralgen.lanl.gov) indicate

207 n DCs stimulated with different serotypes of A. actinomycetemcomitans or P. gingivalis is TLR2 or TLR

208 y DCs stimulated with different serotypes of A. actinomycetemcomitans or P. gingivalis is Toll-like r

209 The carrier status of A. actinomycetemcomitans at the individual level was det

210 We constructed a mutant strain of A. actinomycetemcomitans that contained a transposon ins

211 t possible to transform nearly any strain of A. actinomycetemcomitans, and allelic exchange has prove

212 e sequence of a serotype b non-JP2 strain of A. actinomycetemcomitans.

213 response to the challenge by two strains of A. actinomycetemcomitans (P = 0.018 and P = 0.046).

214 stribution of the GEIs among test strains of A. actinomycetemcomitans was determined by PCR analysis

215 Several strains of A. actinomycetemcomitans, including different serotypes,

216 of both wild-type and morC mutant strains of A. actinomycetemcomitans.

217 ession of novel appendages on the surface of A. actinomycetemcomitans that mediate the adhesion of th

218 t study was to measure the susceptibility of A. actinomycetemcomitans biofilms to detachment and kill

219 me points over 7 h to assess the transfer of A. actinomycetemcomitans from teeth or BECs to HA.

220 Transfer of A. actinomycetemcomitans to HA was not seen in subjects

221 nomycetemcomitans on BECs showed transfer of A. actinomycetemcomitans to HA.

222 on of AAI-1 was found to cause truncation of A. actinomycetemcomitans genes at the insertion site.

223 gh (Rv) and isogenic smooth (Sv) variants of A. actinomycetemcomitans cultured in half-strength and f

224 volved in biofilm formation and virulence of A. actinomycetemcomitans.

225 Furthermore, in studies on A. actinomycetemcomitans leukotoxin workers should now c

226 In early work on A. actinomycetemcomitans workers concluded that this bac

227 Seventy-one A. actinomycetemcomitans-negative and 63 A. actinomycete

228 Only A. actinomycetemcomitans grew after 36 h when peg biofil

229 Opsonized A. actinomycetemcomitans strain Y4 was incubated with th

230 MSP for detection frequency of key pathogen A. actinomycetemcomitans.

231 of LPS derived from the periodontal pathogen A. actinomycetemcomitans can induce severe alveolar bone

232 The periodontal pathogen A. actinomycetemcomitans has been known to exhibit varia

233 All targeted periodontal pathogens (A. actinomycetemcomitans, P. gingivalis, T. forsythia, o

234 en and nitrogen intermediates in periodontal A. actinomycetemcomitans infection and progression to pe

235 tor, we sought to detect and study potential A. actinomycetemcomitans proteins that interact with Ltx

236 we constructed a hyper-leukotoxin producing A. actinomycetemcomitans strain and identified a termina

237 the possible role of the CDT as a prominent A. actinomycetemcomitans virulence factor in periodontal

238 We concluded that PGA protects A. actinomycetemcomitans cells from detachment and killi

239 ll line, GMSM-K, were exposed to recombinant A. actinomycetemcomitans CDT.

240 owever, longitudinal cohort studies relating A. actinomycetemcomitans to initiation of LAP have not b

241 Forty-seven A. actinomycetemcomitans strains of serotypes a through

242 The RbsB/AI-2 complex was thermostable since A. actinomycetemcomitans AI-2 could not be recovered by

243 At vulnerable sites, A. actinomycetemcomitans, Streptococcus parasanguinis, a

244 Some A. actinomycetemcomitans strains may harbor GEIs, which

245 y formation, and periodontitis severity than A. actinomycetemcomitans.

246 While it is clear that A. actinomycetemcomitans responds to precise cues that a

247 Here, we demonstrate that A. actinomycetemcomitans Cdt kills proliferating and non

248 These results demonstrate that A. actinomycetemcomitans promotes the S. parasanguinis b

249 nce for lactate exists despite the fact that A. actinomycetemcomitans grows faster and obtains higher

250 Colocalization studies indicated that A. actinomycetemcomitans bound to type I collagen.

251 We report that A. actinomycetemcomitans promoted biofilm formation of S

252 Recently, we reported that A. actinomycetemcomitans is beta-hemolytic on certain gr

253 Coculture studies reveal that A. actinomycetemcomitans utilizes lactate produced by th

254 Here, we show that A. actinomycetemcomitans LsrB protein competitively inhi

255 We suggest that A. actinomycetemcomitans Cu,Zn SOD may protect both bact

256 These results suggest that A. actinomycetemcomitans possesses two proteins that dif

257 Together, our results strongly suggest that A. actinomycetemcomitans rcpB is essential in the contex

258 More recent reports have suggested that A. actinomycetemcomitans does have the potential to be b

259 he addition of 50 mM ribose, suggesting that A. actinomycetemcomitans AI-2 and ribose bind at the sam

260 rentially regulated in vivo, suggesting that A. actinomycetemcomitans in vivo metabolism is distinct

261 and CdtC may have clinical relevance for the A. actinomycetemcomitans Cdt.

262 With differing constellations of genes, the A. actinomycetemcomitans clades may have evolved distinc

263 re resistant to the cytotoxic effects of the A. actinomycetemcomitans CDT.

264 n a defined medium, approximately 14% of the A. actinomycetemcomitans genes were differentially regul

265 ry genes accounted for 14.1% to 23.2% of the A. actinomycetemcomitans genomes, with a majority belong

266 Together, our results indicate that the A. actinomycetemcomitans TadV protein is a member of a n

267 to remain healthy (survive) compared to the A. actinomycetemcomitans-positive test group (P = 0.0001

268 ctinomycetemcomitans-positive as compared to A. actinomycetemcomitans-negative students remained heal

269 cted LFKO(-/-) mice were more susceptible to A. actinomycetemcomitans-induced alveolar bone loss, wit

270 onsidering edentulism and low serum titer to A. actinomycetemcomitans as risk indicators for chronic

271 er-lacZ transcriptional fusions in wild-type A. actinomycetemcomitans and DeltaihfA and DeltaihfB mut

272 ld World primates, as seen in both wild-type A. actinomycetemcomitans and E. coli expressing ApiA (P

273 Pretreatment of wild-type A. actinomycetemcomitans cells with anti-ApiA antiserum

274 Inactivation of lsrB in wild-type A. actinomycetemcomitans or in an isogenic RbsB-deficien

275 In addition, biofilm growth by wild-type A. actinomycetemcomitans was reduced in the presence of

276 and an aae apiA double mutant with wild-type A. actinomycetemcomitans.

277 rcpB formed biofilms equivalent to wild-type A. actinomycetemcomitans.

278 where the three-organism consortium (versus A. actinomycetemcomitans alone) was detected, the specif

279 Viable A. actinomycetemcomitans biofilm was successfully establ

280 howed that in contrast to the accepted view, A. actinomycetemcomitans leukotoxin can indeed destroy e

281 In vitro, A. actinomycetemcomitans desorbed from BECs and transfer

282 In vivo, A. actinomycetemcomitans colonized HA within 6 h and thu

283 comitans positive for teeth only, and 3 were A. actinomycetemcomitans-negative controls) had two mand

284 Thirteen volunteers (5 were A. actinomycetemcomitans positive for buccal epithelial

285 al epithelial cells [BECs] and teeth, 5 were A. actinomycetemcomitans positive for teeth only, and 3

286 results describe a novel animal model where A. actinomycetemcomitans biofilm was established in vitr

287 analysis was performed to determine whether A. actinomycetemcomitans-positive as compared to A. acti

288 Streptococcus and Actinomyces species, while A. actinomycetemcomitans-positive subjects with BL had h

289 ofiling of S. parasanguinis co-cultured with A. actinomycetemcomitans revealed a significant decrease

290 onor B cells from normal rats immunized with A. actinomycetemcomitans were transferred via tail vein

291 e mast cells and macrophages, incubated with A. actinomycetemcomitans, either opsonized or not, with

292 L/6 wild-type mice were orally infected with A. actinomycetemcomitans and analyzed for bacterial colo

293 Oral infection with A. actinomycetemcomitans increased LF levels in periodon

294 es of S. gordonii with P. gingivalis or with A. actinomycetemcomitans are more pathogenic in animal m

295 Sixteen of 63 subjects with A. actinomycetemcomitans developed BL (the other 47 subj

296 ans developed BL (the other 47 subjects with A. actinomycetemcomitans had no BL).

297 All 5 subjects with A. actinomycetemcomitans on BECs showed transfer of A. a

298 comitans to HA was not seen in subjects with A. actinomycetemcomitans on teeth only.

299 anium implants were inoculated in vitro with A. actinomycetemcomitans, establishing a biofilm for 1 t

300 Students without A. actinomycetemcomitans at baseline had a significantly