ライフサイエンスコーパス: gonococcal

1 entous phage can induce antibodies with anti-gonococcal activity and that phage proteins may be a can

2 ATCC 33323, or L. gasseri ATCC 9857 reduced gonococcal adherence by nearly 50%.

3 s subsequently produced and shown to inhibit gonococcal adherence to epithelial cells in a dose-depen

4 the healthy human vaginal tract, can inhibit gonococcal adherence to epithelial cells in culture.

5 dition, methanol-fixed L. jensenii inhibited gonococcal adherence to live epithelial cells, indicatin

6 ound no evidence that C. muridarum increases gonococcal adherence to, or invasion of, immortalized mu

7 of L. jensenii involved in the inhibition of gonococcal adherence.

8 t of lead compounds for optimization of anti-gonococcal agents.

9 Here, we demonstrated that gonococcal AmiC can act on macromolecular PG to liberate

10 ion to displaying high basal activity on PG, gonococcal AmiC can utilize metal ions other than the zi

11 Thus gonococcal AmiC has distinct differences from related en

12 is partly due to ampG, since replacement of gonococcal ampG with the meningococcal allele reduced PG

13 n, suggesting that the chemistry involved in gonococcal anaerobic UFA synthesis is distinct from that

14 in which methods for the diagnosis of rectal gonococcal and chlamydial infection are optimal.

15 dered to be acceptable for identification of gonococcal and chlamydial infections from urine samples,

16 Over 60% and 80% of gonococcal and chlamydial infections, respectively, amon

17 ment, previously identified elsewhere in the gonococcal and meningococcal genomes, was present in the

18 ntial to offer broad protection against both gonococcal and meningococcal infections.

19 and the maintenance of variant GGIs in some gonococcal and meningococcal isolates.

20 -year incidence rate of PID was 10.9% and of gonococcal and/or chlamydial cervicitis was 21.9%.

21 rd ratios for the comparison of trichomonal, gonococcal, and chlamydial infection incidence in partic

22 ssed by Gram stain and incident trichomonal, gonococcal, and/or chlamydial genital infection.

23 levated risk for acquisition of trichomonal, gonococcal, and/or chlamydial genital infection.

24 old increased risk for incident trichomonal, gonococcal, and/or chlamydial infection (adjusted hazard

25 with a positive test result for trichomonal, gonococcal, and/or chlamydial infection.

26 13.3% by positive detection of trichomonal, gonococcal, and/or chlamydial infection.

27 The rise in gonococcal antibiotic resistance and the threat of untre

28 eviously shown to regulate the expression of gonococcal antimicrobial efflux systems.

29 nce typing, and challenges posed by emerging gonococcal antimicrobial resistance.

30 could bridge bacteria to CR3 and facilitate gonococcal association with host cells.

31 s, supporting AmiC's purported function as a gonococcal autolysin.

32 To further study the mechanism of gonococcal biofilm formation, we compared transcriptiona

33 on occurs predominantly in the substratum of gonococcal biofilms and that expression of aniA is induc

34 xtends to its ability to disrupt established gonococcal biofilms through degradation of the DNA in th

35 (LOS) epitope recognized mAb 2C7 attenuates gonococcal burden in the mouse vaginal colonization mode

36 We show that only gonococcal, but not meningococcal, LNT LOS sialylation e

37 Here we showed that a gonococcal catalase (kat) mutant in strain MS11 was more

38 respiratory burst during infection and that gonococcal catalase and the MntC protein confer an unide

39 Here we assessed the importance of gonococcal catalase in a surrogate model of female genit

40 A gonococcal catalase mutant and a catalase, cytochrome C

41 Mutagenized TbpAs were expressed on the gonococcal cell surface and maintained wild-type transfe

42 crease in T-cell populations observed during gonococcal cervicitis.

43 tment of mice with IL-12 microspheres during gonococcal challenge led to faster clearance of infectio

44 fore, we propose a mechanism where a low MOI gonococcal challenge results in diminished AP-1 activity

45 IL-8 induction resulting from gonococcal challenge was shown to require NF-kappaB acti

46 76, 95% confidence interval: 0.42, 1.38) nor gonococcal/chlamydial genital infection (adjusted hazard

47 n between douching and development of PID or gonococcal/chlamydial genital infection among predominan

48 ncy of douching immediately preceding PID or gonococcal/chlamydial genital infection was not differen

49 Associations between douching and PID or gonococcal/chlamydial genital infections were assessed b

50 mm/hour, white blood cell count >10,000, or gonococcal/chlamydial lower genital infection.

51 mm/hour, white blood cell count >10,000, or gonococcal/chlamydial lower genital tract infection.

52 was likely acquired and integrated into the gonococcal chromosome by site-specific recombination and

53 veral predictions of the polyploidy model of gonococcal chromosome organization.

54 difA and difB, is not readily lost from the gonococcal chromosome, the substitution of difB with ano

55 ) and highest for cervical LCR when cervical gonococcal coinfection was detected (91%).

56 vical and urethral inflammation, menses, and gonococcal coinfection) were assessed.

57 ork, we show that deletion of ng1686 affects gonococcal colony morphology but not cell morphology and

58 tion, 8 participants had positive pharyngeal gonococcal cultures, and 4 had positive rectal cultures.

59 found associated with PMNs, suggesting that gonococcal defences against oxidative stress are crucial

60 had acquired by gene conversion the complete gonococcal denitrification norB-aniA gene cassette, and

61 lude three genes implicated in the truncated gonococcal denitrification pathway: aniA, norB, and narQ

62 tion tests (NAATs) for rectal chlamydial and gonococcal diagnosis.

63 al cells is important to the pathogenesis of gonococcal disease and may contribute to the persistence

64 sting sequelae, prompting the reemergence of gonococcal disease as a leading global health concern.

65 hormones potentially modulate the course of gonococcal disease in women.

66 seria, the epidemiology of meningococcal and gonococcal disease, and mechanisms of Neisseria pathogen

67 severe restriction of treatment options for gonococcal disease.

68 e female genital tract mediate the course of gonococcal disease.

69 ected to be important in the pathogenesis of gonococcal disease.

70 gonococcal Fur- and iron-regulated genes in gonococcal disease.

71 pilus-associated proteins are necessary for gonococcal DNA uptake.

72 s in stationary phase, indicating that other gonococcal enzymes are also involved in this process.

73 e significantly to studies of host immunity, gonococcal epidemiology, and pathogenesis.

74 Gonococcal fatty acid profiles confirmed that NGO1024 wa

75 This study demonstrated that the gonococcal FbpABC transport system is required for utili

76 s of resistance mechanisms that may increase gonococcal fitness and therefore the potential for sprea

77 isolated gyrA(91/95) and parC86 mutations on gonococcal fitness.

78 Gonococcal fluoroquinolone resistance emerged more rapid

79 lectively, our studies have established that gonococcal Fur functions as an activator of gene transcr

80 study we have demonstrated expression of the gonococcal fur gene in vitro, in human cervical epitheli

81 studies confirmed that the expression of the gonococcal fur gene was repressed during growth under ir

82 e genes exhibited reduced transcription in a gonococcal fur mutant strain.

83 itro findings and point toward a key role of gonococcal Fur- and iron-regulated genes in gonococcal d

84 The gonococcal Fur-activated genes displayed variable transc

85 f its four intrinsic 16S rRNA genes with the gonococcal gene.

86 indicate that transcriptional regulation of gonococcal genes by MtrR is centrally involved in determ

87 lify, by reverse transcriptase PCR (RT-PCR), gonococcal genes known to be regulated by iron and Fur (

88 er MtrR can exert regulatory action on other gonococcal genes, we performed a whole-genome microarray

89 The 57-kb gonococcal genetic island (GGI) encodes a type IV secret

90 e found that mutations in three genes in the gonococcal genetic island (GGI) reduced the ability of a

91 FA1090, however, lacks the gonococcal genetic island (GGI) that is present in the m

92 ins of Neisseria gonorrhoeae carry the 57-kb gonococcal genetic island (GGI), as do a few strains of

93 -MtrE efflux-pump system during experimental gonococcal genital-tract infection and also illustrate a

94 The completion of the gonococcal genome sequence has facilitated the identific

95 b 2C7 showed functional activity against all gonococcal HepI LOS structures defined by various lgtA/C

96 gulated tbpA and tbpB genes are expressed in gonococcal infection and that male subjects with mucosal

97 ensitive for the detection of chlamydial and gonococcal infection at the rectal site than is culture.

98 ined from female subjects with uncomplicated gonococcal infection corroborated our in vitro findings

99 specific vaginal bacteria and chlamydial or gonococcal infection detected by strand displacement ass

100 n with the same serovar can occur, and prior gonococcal infection does not alter the Ig response upon

101 of participants with a laboratory-confirmed gonococcal infection during the 36-month follow-up.

102 the contributions of MisR and MisS (CpxA) to gonococcal infection in a murine model of cervicovaginal

103 d genes are expressed in vivo during mucosal gonococcal infection in men, which suggests that this or

104 not constitutive activation is required for gonococcal infection in mice.

105 erefore the potential for spread, (b) use of gonococcal infection in the animal model system to study

106 Gonococcal infection induced a significant increase in s

107 The role of autolysis during gonococcal infection is not known, but possible advantag

108 Although gonococcal infection of B cells produced small amounts o

109 that an intact MisRS system is required for gonococcal infection of mice.

110 irectly influences B cells, we observed that gonococcal infection prolonged viability of primary huma

111 Neisseria gonorrhoeae to cause disseminated gonococcal infection requires that such strains resist t

112 In this work, a cell culture model of gonococcal infection was adapted to examine the effects

113 inal pH, positive whiff test, and concurrent gonococcal infection were positively associated with TV

114 genic diversity and allow the persistence of gonococcal infection within the human population.

115 Symptomatic gonococcal infection, caused by the pathogen Neisseria g

116 Symptomatic gonococcal infection, caused exclusively by the human-sp

117 During and after gonococcal infection, local and systemic antigonococcal

118 regulated genes in vivo during uncomplicated gonococcal infection, we examined gene expression profil

119 A microarrays and a tissue culture model for gonococcal infection, we examined global changes in gene

120 oluble 17beta-estradiol to promote long-term gonococcal infection.

121 rations in host innate responses may enhance gonococcal infection.

122 erapeutic and prophylactic compounds against gonococcal infection.

123 play a role in tubal scarring in response to gonococcal infection.

124 ffects of H(2)O(2)-producing lactobacilli on gonococcal infection.

125 lain species-specific restriction of natural gonococcal infection.

126 mens from female subjects with uncomplicated gonococcal infection.

127 a key arm of innate immune defenses against gonococcal infection.

128 ge of nucleic acid amplification testing for gonococcal infection.

129 the human host, the only known reservoir for gonococcal infection.

130 BV), often without concomitant chlamydial or gonococcal infection.

131 implications for understanding asymptomatic gonococcal infection.

132 immune responses in a mouse model of genital gonococcal infection.

133 sion of IgD(+)CD27(+) B cells in response to gonococcal infection.

134 o = 0.50; 95% CI, 0.28 to 0.88; P = .02) and gonococcal infections (48 vs 54 participants, respective

135 and public health strategy for management of gonococcal infections and antimicrobial resistance.

136 her insights into the species specificity of gonococcal infections and proof-of-concept of a novel th

137 ere calculated separately for chlamydial and gonococcal infections and were stratified by assay and p

138 ay have resulted in decreased chlamydial and gonococcal infections at the population level.

139 Gonococcal infections cause significant morbidity, parti

140 Gonococcal infections do not elicit protective immunity,

141 nfection and that male subjects with mucosal gonococcal infections exhibit antibodies to these protei

142 ariable pathophysiology of meningococcal and gonococcal infections given that after an initial exposu

143 Here, we demonstrate that women with gonococcal infections have levels of sialidases present

144 and Prevention STD treatment guidelines for gonococcal infections in adolescents and adults.

145 the evidence on screening for chlamydial and gonococcal infections in asymptomatic patients from stud

146 specificity of polymerase chain reaction to gonococcal infections in men was 90.4%.

147 rnative treatment regimen, and management of gonococcal infections in persons with severe cephalospor

148 e regarding the prevalence of chlamydial and gonococcal infections in the general young adult populat

149 ions in men; and 55.6%, 91.3%, and 84.9% for gonococcal infections in women.

150 Specificity for gonococcal infections was >/= 99.8%.

151 es were evaluated, and 281 chlamydial and 69 gonococcal infections were identified.

152 ral barriers to screening for chlamydial and gonococcal infections, but most test samples are obtaine

153 In a laboratory model of mixed gonococcal infections, the por type of one strain could

154 To better understand the role of Opa in gonococcal infections, we created and characterized a de

155 et for beta-lactam antibiotics used to treat gonococcal infections.

156 G, which for over 40 years was used to treat gonococcal infections.

157 rkers, a continuing problem for treatment of gonococcal infections.

158 arm of the innate immune system that combats gonococcal infections.

159 nd a collection of strains from disseminated gonococcal infections.

160 96.9 to 100% using LCA for the detection of gonococcal infections.

161 ed to examine the effects of lactobacilli on gonococcal interactions with endometrial epithelial cell

162 nii uses a constitutive component to inhibit gonococcal interactions with epithelial cells.

163 environment and this protein was critical to gonococcal intracellular survival.

164 Lactobacilli also inhibited gonococcal invasion of epithelial cells by more than 60%

165 These results indicate that gonococcal iron- and Fur-regulated tbpA and tbpB genes a

166 Centers for Disease Control and Prevention's Gonococcal Isolate Surveillance Project (GISP) from sent

167 f a combination of routine isolates from the Gonococcal Isolate Surveillance Project and isolates col

168 smitted disease clinic, a participant in the Gonococcal Isolate Surveillance Project, during 2009.

169 Centers for Disease Control and Prevention's Gonococcal Isolate Surveillance Project.

170 mary outcome measures included percentage of gonococcal isolates resistant to antimicrobials used to

171 This cluster of genetically related gonococcal isolates with decreased ceftriaxone susceptib

172 Both BamD and BamE are expressed in diverse gonococcal isolates, under host-relevant conditions, and

173 serum resistance mediated by sialylation of gonococcal L1 and LNT LOS occurs by different mechanisms

174 Sialylation of gonococcal lipo-oligosaccharide, or expression of porin

175 A gonococcal lipooligosaccharide epitope defined by the mA

176 Although gonococcal LNT LOS sialylation enhances binding of the a

177 Gonococcal LOS from the 5 strains and lipopolysaccharide

178 ncodes a protein mediating PEA addition onto gonococcal LOS.

179 can result in desialylation of (sialylated) gonococcal LOS.

180 tabolism in this bacterium to understand how gonococcal manipulation of NO concentration may influenc

181 ellular DNA is an essential component of the gonococcal matrix.

182 found in the FA1090 genome, suggesting that gonococcal MMC is not methyl directed.

183 These results show that gonococcal MMC repairs mismatches and small insertion/de

184 Gonococcal mutants deficient in MtrA, an activator of th

185 Isogenic gonococcal mutants in which the lgt required for mAb 2C7

186 When expressed in Escherichia coli, gonococcal NarQ and chimaeras of E. coli and gonococcal

187 gonococcal NarQ and chimaeras of E. coli and gonococcal NarQ are ligand-insensitive and constitutivel

188 Estimates were similar for trichomonal-only, gonococcal-only, and chlamydial-only infection outcomes.

189 Douching has been linked to gonococcal or chlamydial cervicitis and pelvic inflammat

190 The secondary end point was newly acquired gonococcal or chlamydial infection.

191 in vitro, which is facilitated by either the gonococcal or E. coli RecA proteins or high pH, and auto

192 istant N gonorrhoeae through augmentation of gonococcal outbreak surveillance and identification of p

193 ooligosaccharide (LOS) is a component of the gonococcal outer membrane that induces innate immunity t

194 rhoeae porin protein Por are needed to study gonococcal pathogenesis in the natural host and to class

195 tigating the contribution of Opa proteins to gonococcal pathogenesis is complicated by high-frequency

196 murine infection to study certain aspects of gonococcal pathogenesis.

197 The purified endopeptidase degraded gonococcal peptidoglycan in vitro, cutting the peptide c

198 gococcal PG recycling is more efficient than gonococcal PG recycling.

199 terone functioned in an additive manner with gonococcal phospholipase D to augment Akt kinase activit

200 al-time RT-PCR assay was designed to measure gonococcal pilin antigenic variation (SQ-PCR Av assay).

201 that these recombinases are not involved in gonococcal pilin variation, DNA transformation, or DNA r

202 The gonococcal pilus undergoes antigenic variation through h

203 ntified 21 prevalent strains in this diverse gonococcal population, each infecting between 20 and 124

204 actor H binding to meningococci that express gonococcal Por.

205 sialylated) that did not bind factor H with gonococcal Por1B augmented factor H binding.

206 Gonococcal Por1B introduced in the background of an unsi

207 o unsialylated meningococci transfected with gonococcal Por1B was similar to the sialylated counterpa

208 lylated meningococcal mutants that possessed gonococcal Por1B were resistant to complement-mediated k

209 Conversely, replacing gonococcal Por1B with meningococcal PorB abrogated facto

210 se effects of lipid A PEA on C4BP binding to gonococcal PorB and serum resistance were simulated when

211 orB and serum resistance were simulated when gonococcal PorB was expressed in a meningococcal backgro

212 rB.1B, we discovered that strains expressing gonococcal PorB.1B in the presence of sialylated lipooli

213 ains expressing either meningococcal fHbp or gonococcal PorB.1B, we discovered that strains expressin

214 ontribute to the antiapoptotic effect of the gonococcal porin, PIB.

215 d, cloned, and insertionally inactivated the gonococcal priA homologue.

216 R is shown to be an additional member of the gonococcal RecF-like recombination pathway.

217 s indirect inactivation by nitric oxide of a gonococcal repressor, NsrR, identified from a multigenom

218 We obtained data from the Gonococcal Resistance to Antimicrobials Surveillance Pro

219 The capacity of polyamines to increase gonococcal resistance to cationic antimicrobial peptides

220 lamine (PEA) decoration of lipid A increases gonococcal resistance to complement-mediated bacteriolys

221 addition, we found that polyamines increase gonococcal resistance to complement-mediated killing by

222 pump operon and, as a consequence, levels of gonococcal resistance to host antimicrobials (e.g., anti

223 al repressor of the mtrCDE operon, increases gonococcal resistance to these agents.

224 t that polyamines can significantly increase gonococcal resistance to two structurally diverse cation

225 The constitutively expressed gonococcal rmp gene was used as a positive control.

226 d in adherent gonococci, two are part of the gonococcal RpoH regulon.

227 (FISH) probes specific for meningococcal and gonococcal rRNA were used to demonstrate the expression

228 heptose (Hep) glycan substitutions influence gonococcal serum resistance.

229 The ability of gonococcal sialylated LNT to bind factor H confers high-

230 fection of B cells produced small amounts of gonococcal-specific IgM, IgM specific for irrelevant Ags

231 s as the primary target of Opa proteins, the gonococcal specificity for this human family of receptor

232 usly characterized in an FA19 penA mtrR penB gonococcal strain (PR100) as a spontaneous mutation that

233 Each gonococcal strain carried one of three different alleles

234 t of crgA (DeltacrgA) in the serum-sensitive gonococcal strain F62.

235 t the outer membrane transporter FetA allows gonococcal strain FA1090 to utilize the xenosiderophore

236 this study, we investigated the survival of gonococcal strain FA1090 within ME180 human cervical epi

237 ngococcal strain Z2491 (ET-IV; ST-4) and the gonococcal strain FA1090.

238 ression of FbpABC was required for growth of gonococcal strain FA19 in the presence of enterobactin a

239 hosphoethanolamine (PEA) from the lipid A of gonococcal strain FA19 results in increased sensitivity

240 erobactin and salmochelin promoted growth of gonococcal strain FA19.

241 21%) suggested the presence of more than one gonococcal strain.

242 ccharide beta-chain did not impact levels of gonococcal (strain FA19) resistance to normal human seru

243 OS or whole bacteria, compared with LOS from gonococcal strains 1291 and GC56 with reduced levels of

244 of the strains, meningococcal strain 89I and gonococcal strains 1291 and GC56, representing high, int

245 explaining the absence of the GGI from some gonococcal strains and the maintenance of variant GGIs i

246 ) is an epidemiological tool that classifies gonococcal strains based on sequence differences in regi

247 Several gonococcal strains bind the classical complement pathway

248 rt that LOS from different meningococcal and gonococcal strains have different potencies to activate

249 s required for C4BP binding to Por1B-bearing gonococcal strains MS11 and 1291 but not to FA19 (Por1A)

250 uman infection, is on the rise worldwide and gonococcal strains resistant to many antibiotics are eme

251 We show that only those gonococcal strains that bind C4BP require properdin for

252 Loss of PEA from lipid A in three additional gonococcal strains that expressed diverse PorB molecules

253 Ab-mediated complement-dependent killing of gonococcal strains that inhibit the classical pathway by

254 An exception was serotype Por1B-bearing gonococcal strains that previously had been used success

255 were cross-bactericidal against heterologous gonococcal strains, whereas TbpB-specific antibodies wer

256 F-kappaB activity than released fragments in gonococcal supernatants and tended to induce less interl

257 imilar modest ligand-blocking effects on the gonococcal surface but different effects in Escherichia

258 els of gonococcal transmission, new tools in gonococcal surveillance may provide useful data to aid t

259 amines in genital mucosal fluids may enhance gonococcal survival during infection by reducing bacteri

260 The MtrC-MtrD-MtrE system is important for gonococcal survival in the murine genital tract, and der

261 antimicrobial peptides, suggesting a role in gonococcal survival in vivo Here, we evaluated the contr

262 In vivo testing of the role of catalase in gonococcal survival is critical since several physiologi

263 acquisition and GGI-encoded gene products in gonococcal survival within cervical epithelial cells.

264 ible nitric oxide synthase activity promoted gonococcal survival within pex cells.

265 ng the importance of D-lactate metabolism in gonococcal survival.

266 poH-regulated genes also modulates levels of gonococcal susceptibility to H(2)O(2).

267 d to repress rpoH expression and to increase gonococcal susceptibility to hydrogen peroxide (H(2)O(2)

268 centrally involved in determining levels of gonococcal susceptibility to penicillin and provides a f

269 epressor of the efflux pump operon, decrease gonococcal susceptibility to penicillin.

270 ssion of two other loci that are involved in gonococcal susceptibility to penicillin: ponA, which enc

271 inactivation of lptA, resulted in increased gonococcal susceptibility to polymyxin B, as reported pr

272 genes (kat, ccp, and mntC) does not increase gonococcal susceptibility to the phagocytic respiratory

273 These results suggest that the gonococcal T4SS may be present in single copy per cell a

274 Unlike other gonococcal T4SS proteins we have investigated, protein l

275 Similar to other F-like T4SSs, the gonococcal T4SS requires a putative membrane protein, Tr

276 nal studies showed that in contrast with the gonococcal T4SS, the meningococcal T4SS does not secrete

277 Using a three-dimensional structure of gonococcal TbpA, we investigated two hypotheses, i.e., t

278 latory data demonstrating that production of gonococcal TdfH and TdfJ are unresponsive to or upregula

279 In this study, we found that production of gonococcal TdfH is both Zn and Zur repressed.

280 Four gonococcal TdTs facilitate utilization of iron or iron c

281 ding studies, was more often associated with gonococcal the most common VR types.

282 h to examine the role of NrrF in controlling gonococcal transcription.

283 We investigated the immunogenicity of gonococcal transferrin binding protein B (TbpB) expresse

284 inding proteins (TbpA and TbpB) comprise the gonococcal transferrin receptor and are considered poten

285 The gonococcal transferrin receptor is composed of two disti

286 The gonococcal transferrin-iron uptake system is composed of

287 ides insight into previous investigations of gonococcal transformation.

288 impeded development of operational models of gonococcal transmission, new tools in gonococcal surveil

289 e most well-studied type IV filaments is the gonococcal type IV pilus (GC-T4P) from Neisseria gonorrh

290 The gonococcal type IV secretion system secretes DNA during

291 ride bactericidal monoclonal Ab (mAb) 2C7, a gonococcal vaccine candidate Ab, attenuates vaginal colo

292 consideration in evaluating the efficacy of gonococcal vaccine candidates.

293 e encoded proteins could form the basis of a gonococcal vaccine, rabbits were orally infected with S.

294 ther impetus for use of the 2C7 epitope in a gonococcal vaccine.

295 y how blocking Abs influence the efficacy of gonococcal vaccines.

296 We observed that gonococcal variants that produced type IV pili secreted

297 able, suggesting that they are essential for gonococcal viability.

298 ence of BamD, but not BamE, is essential for gonococcal viability.

299 reviously identified the NG1686 protein as a gonococcal virulence factor that protects against both n

300 H directly binds calprotectin, which enables gonococcal Zn accumulation in a TdfH-dependent manner an