ライフサイエンスコーパス: chlamydial

1 spectively, may allow the plasmid to promote chlamydial adaptation to varied animal tissue environmen

2 tected macaques proliferated against soluble chlamydial Ag.

3 ted here for the first time, the predominant chlamydial agent was C. gallinacea representing 63.8% of

4 ary to homologues from free-living bacteria, chlamydial AmiA uses lipid II as a substrate and has dua

5 d its use and may have resulted in decreased chlamydial and gonococcal infections at the population l

6 SPSTF reviewed the evidence on screening for chlamydial and gonococcal infections in asymptomatic pat

7 best indicator of B-cell epitope regions for chlamydial and published datasets.

8 sociates of amoebae were classified to order Chlamydiales and genus Burkholderia-Caballeronia-Parabur

9 ars of speculation and debate concerning the chlamydial anomaly and are the strongest evidence so far

10 ydial species have proven unsuccessful (the 'chlamydial anomaly').

11 The "chlamydial anomaly," first coined by James Moulder, desc

12 ibits cytokinesis, a phenomenon known as the chlamydial anomaly.

13 , the above observations have demonstrated a chlamydial antigen-independent immune mechanism for regu

14 A variety of chlamydial antigens are being used to help differentiate

15 Cross-reactivity of classical chlamydial antigens compromises Chlamydia (C.) pneumonia

16 y to Chlamydia trachomatis Identification of chlamydial antigens that induce interferon gamma (IFN-)

17 t Escherichia coli expressing a panel of 275 chlamydial antigens.

18 The pathogen responsible was not chlamydial, as is often found in epitheliocystis, but a

19 monstrated a critical role of the plasmid in chlamydial ascending infection.

20 evaluate the contribution of the plasmid to chlamydial ascension and activation of tubal inflammatio

21 TC0668 as novel genetic factors involved in chlamydial attachment and pathogenicity, respectively, a

22 al cells was associated with a deficiency in chlamydial attachment to cells.

23 icient mice developed reduced pathology, the chlamydial burden and immune cell infiltration were dete

24 ce at 1 dpi restored lung T cell numbers and chlamydial burden at 12 dpi to levels seen in infected c

25 Although chlamydial burden was similar in WT and Il1a(-/-) oviduc

26 ase-11-deficient mice, we observed increased chlamydial burdens in the upper genital tract, which cor

27 to Spiroplasma and Mycoplasma genera, one to chlamydial 'Candidatus Syngnamydia', and one to bacteroi

28 a (obligates) belonging to Rickettsiales and Chlamydiales cause diseases in hundreds of millions of p

29 BP2 and PBP3 in regulating specific steps in chlamydial cell division have not been described in othe

30 as been proposed as playing a unique role in chlamydial cell division.

31 nes in cervical secretions from women having chlamydial cervical infection alone (n = 92) or both cer

32 Thus, we propose that chlamydial chromosomal-gene-encoded genital tract virule

33 l expansion in LNG-treated mice also delayed chlamydial clearance and the resolution of pulmonary inf

34 y not only has revealed that pGP3 is a novel chlamydial colonization factor in the gastrointestinal t

35 but not the large intestine, indicating that chlamydial colonization in different regions of the gast

36 tions to reveal the impact of the plasmid on chlamydial colonization in distinct regions of gastroint

37 of gastric and intestinal effectors and (ii) chlamydial colonization in small intestine was highly de

38 of chlamydial induction of hydrosalpinx with chlamydial colonization in the gastrointestinal tract th

39 The cryptic plasmid pCM is critical for chlamydial colonization in the gastrointestinal tract.

40 The cryptic plasmid is important for chlamydial colonization in the gastrointestinal tract.

41 tract, but the host immunity that regulates chlamydial colonization in the gut remains unclear.

42 leukin 22 (IL-22) signaling pathways rescued chlamydial colonization in the small intestine.

43 Correlation of chlamydial colonization of the gastrointestinal tract wi

44 an intracolon inoculation, the dependence of chlamydial colonization on plasmid increased over time.

45 culation, the plasmid significantly improved chlamydial colonization.

46 recently proposed as the pathogenic basis of chlamydial complications.

47 Members of the order Chlamydiales comprise a group of exquisitely evolved par

48 ith the lack of a regulatory domain in AmiA, chlamydial CPn0902, annotated as NlpD, is a carboxypepti

49 Strains with nonsense mutations in chlamydial cytotoxins, guaBA-add, and a phospholipase D

50 rk demonstrated the bifunctional activity of chlamydial DapF in vitro and in a heterologous system (E

51 Here, we show that the chlamydial deubiquitinating enzyme (Cdu) 1 localizes in

52 Altogether, our data indicate that chlamydial development has a dynamic relationship with t

53 us, support chlamydial lipid acquisition and chlamydial development.

54 supercoiling levels during the intracellular chlamydial developmental cycle are regulated by unusual

55 egulation of heat shock genes throughout the chlamydial developmental cycle, but the level of repress

56 ter regulator of late gene expression in the chlamydial developmental cycle.

57 of C. trachomatis, and inclusions containing chlamydial developmental forms were visualized by fluore

58 indicating a critical role of the plasmid in chlamydial differentiation into infectious particles in

59 This finding may provide new targets for chlamydial disease biomarkers and prevention.

60 nic inflammation often associated with human chlamydial disease.

61 ntrollers," i.e., animals without detectable chlamydial DNA in the fimbriae at weeks 5 and 12.

62 e in association with STING, indicating that chlamydial DNA is most likely recognized outside the inc

63 In addition, we have shown that the chlamydial effector protein, CPAF, which is secreted int

64 s in general, leading to the uptake of fewer chlamydial elementary bodies and diminished turnover of

65 cestor of malaria parasites once contained a chlamydial endosymbiont.

66 T3SSs in contact with host membranes during chlamydial entry and intracellular replication, and the

67 with homology to factors known to facilitate chlamydial entry to the host cell.

68 and the pGP3-dependent resistance may enable chlamydial evasion of the female lower genital tract bar

69 FabI) of C. trachomatis to determine whether chlamydial FASII is essential for replication within the

70 ated that the plasmid may be able to improve chlamydial fitness in different gut regions via differen

71 t azithromycin is far less effective against chlamydial gastrointestinal infection than against genit

72 We show that pmpD is not an essential chlamydial gene and the pmpD null mutant has no detectab

73 Temporal expression of chlamydial genes during the intracellular infection is p

74 s new genetic tools began to emerge to study chlamydial genes in vivo, we speculated as to what degre

75 roughs have led to a steady expansion of the chlamydial genetic tool kit, there are still roads left

76 An important question in the study of chlamydial genital tract disease is why some women devel

77 All chlamydial genomes contain the coding capacity for a non

78 Rates of chlamydial, gonococcal, and syphilis infection continue

79 ne of p53, which, in turn, severely affected chlamydial growth and had a marked effect on the mitocho

80 We show that these drugs block chlamydial growth and induce changes in morphology and t

81 ncreased amounts of proteins associated with chlamydial growth and replication, including transferrin

82 Although the plasmid is not critical for chlamydial growth in vitro, its role in chlamydial patho

83 nd Pgp3, -5, and -7 as being dispensable for chlamydial growth in vitro.

84 multiplicity of infection (MOI), and optimal chlamydial growth occurs in macrophages infected at an M

85 However, whether NO is able to arrest chlamydial growth remains unclear.

86 es infected at a moderate MOI, implying that chlamydial growth was blocked by activated defense mecha

87 and activity in infected cells and inhibited chlamydial growth.

88 drazides, which cannot chelate iron, inhibit chlamydial growth.

89 However, activation of the chlamydial gyrase promoter by increased supercoiling is

90 Induction of chlamydial heat shock gene expression by elevated temper

91 ChIP-qPCR method to study the regulation of chlamydial heat shock gene regulation during an intracel

92 This approach allowed us to show that chlamydial heat shock genes are regulated by the transcr

93 Serum anti-chlamydial IgG is not associated with a lowered rate of

94 pulation that functions in antibody-mediated chlamydial immunity.

95 med a cross-sectional analysis of serum anti-chlamydial immunoglobulin G (IgG), behavioral factors, a

96 SNARE proteins mediate fusion events at the chlamydial inclusion and are important for chlamydial li

97 ing eukaryotic vesicular interactions at the chlamydial inclusion and, thus, support chlamydial lipid

98 unctate regions on the cytosolic side of the chlamydial inclusion membrane in association with STING,

99 An in vivo understanding of the secreted chlamydial inclusion membrane protein (Inc) interactions

100 Thus, the chlamydial inclusion serves as an enriched site for a de

101 tage decreases the rate of infection and the chlamydial inclusion size.

102 and is stabilized by deubiquitination at the chlamydial inclusion.

103 in vivo protein-protein interactions at the chlamydial inclusion.

104 Chlamydial inclusions are uncoupled from the endolysosom

105 nonactive CPAF was restricted to within the chlamydial inclusions, regardless of how the infected ce

106 the first mechanistic insights both into how chlamydial Incs hijack host proteins, and how SNX5-relat

107 Chlamydial induction of EMT resulted in the generation o

108 tissue, suggesting that C5 may contribute to chlamydial induction of hydrosalpinx by enhancing inflam

109 tive contributions of these two receptors to chlamydial induction of hydrosalpinx in mice.

110 ceptor TNFR1 play a more significant role in chlamydial induction of hydrosalpinx than those mediated

111 al tract, leading to a better correlation of chlamydial induction of hydrosalpinx with chlamydial col

112 e to CD8 knockout mice significantly reduced chlamydial induction of hydrosalpinx, demonstrating that

113 T cell-deficient mice significantly reduced chlamydial induction of hydrosalpinx, indicating that CD

114 t factor 5 (C5) contributes significantly to chlamydial induction of hydrosalpinx.

115 why the C3(-/-) mice remained susceptible to chlamydial induction of hydrosalpinx.

116 stem, did not affect mouse susceptibility to chlamydial induction of hydrosalpinx.

117 uct infection with inflammatory responses in chlamydial induction of long-lasting hydrosalpinx, sugge

118 Nevertheless, the chlamydial induction of uterine horn/glandular duct dila

119 compared with those with upper genital tract chlamydial infection (13.8% vs 9.5%; P =04), but the CD4

120 more telephone contacts had a lower risk of chlamydial infection (risk ratio = 0.95; 95% CI, 0.90 to

121 ective effector and memory responses against chlamydial infection and demonstrates that an effective

122 ations on the epidemiology and management of chlamydial infection and disease in humans.

123 roteasome-like activity factor), its role in chlamydial infection and pathogenesis remains unclear.

124 cipants with a laboratory-confirmed incident chlamydial infection and percentage of participants with

125 ce depletion of CD4(+) T cells both promoted chlamydial infection and reduced chlamydial pathogenicit

126 Patients with rectal chlamydial infection and signs or symptoms of proctitis

127 been implicated in susceptibility to genital chlamydial infection and the development of tubal pathol

128 of a major category of altered miRNAs during chlamydial infection are key components of the pathophys

129 hildren and adults were monitored for ocular chlamydial infection by polymerase chain reaction.

130 her compared host inflammatory responses and chlamydial infection courses between the hydrosalpinx-re

131 gesting that reduced macrophage responses to chlamydial infection do not always lead to a reduction i

132 TGF-beta signaling pathways cooperate during chlamydial infection for optimal inclusion development a

133 omic profiling of the macrophage response to chlamydial infection highlighted the role of the type I

134 dren in trachoma-endemic communities reduces chlamydial infection in both children and untreated adul

135 T cell-dependent pathogenic mechanism during chlamydial infection in C57BL/6J mice.

136 iPSCs, and confirmed their roles in limiting chlamydial infection in macrophages.

137 S is required for IFN-beta expression during chlamydial infection in multiple cell types.

138 Interestingly, C5 activation was induced by chlamydial infection in oviducts of C3(-/-) mice, explai

139 Chlamydial infection in the lower genital tract can lead

140 of oviduct pathology resulting from genital chlamydial infection in the mouse model.

141 We conclude that adequate live chlamydial infection in the oviduct may be necessary to

142 Their potential impact on the burden of chlamydial infection in the United States, in light of s

143 contributing to the most serious sequelae of chlamydial infection in women: pelvic inflammatory disea

144 reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and

145 Flow cytometry revealed that chlamydial infection induced cell surface expression of

146 e horn dilation, developed in mice following chlamydial infection remains unclear.

147 atified pair-formation transmission model of chlamydial infection to epidemiologic data in the United

148 nses at the cervical mucosa that could limit chlamydial infection to the cervix and/or prevent reinfe

149 trachoma, conjunctival swabs were tested for chlamydial infection using GeneXpert platform, and blood

150 ced IFN-beta expression significantly during chlamydial infection using small interfering RNA and gen

151 Chlamydial infection was detected in the glandular epith

152 Heterosexual individuals with gonorrhea or chlamydial infection were eligible for the intervention.

153 assessed, conjunctival swabs were tested for chlamydial infection, and blood spots were collected on

154 s detected in women with lower genital tract chlamydial infection, compared with those with upper gen

155 To study the human cellular responses to chlamydial infection, researchers have frequently used t

156 significant role for antibody in immunity to chlamydial infection.

157 antly to oviduct pathology following genital chlamydial infection.

158 ment or function during primary or secondary chlamydial infection.

159 Yersinia spp., have an inhibitory effect on chlamydial infection.

160 fine the role of PmpD in the pathogenesis of chlamydial infection.

161 allmark of tubal infertility associated with chlamydial infection.

162 of DNA sensors in IFN-beta expression during chlamydial infection.

163 n between TGF-beta and EGFR signaling during chlamydial infection.

164 ns, and lower fertility rate associated with chlamydial infection.

165 al factor infertility resulting from genital chlamydial infection.

166 blasts and production of ECM proteins during chlamydial infection.

167 han in the comparison condition had incident chlamydial infections (94 vs 104 participants, respectiv

168 eptable for identification of gonococcal and chlamydial infections from urine samples, but are not re

169 Although the concept of persistence in chlamydial infections has been recognized for about 80 y

170 In women, chlamydial infections may cause pelvic inflammatory dise

171 tial data demonstrating treatment failure of chlamydial infections, particularly with azithromycin.

172 re is no FDA-approved treatment specific for chlamydial infections.

173 ammatory disease versus 14.4% (5.9-24.6%) of chlamydial infections.

174 ase severity depends on the virulence of the chlamydial inoculum.

175 cy of FRAEM and reveal a role of TmeA during chlamydial invasion that manifests independently of effe

176 4/CTL0063 is a virulence protein involved in chlamydial invasion.

177 ynthase (iNOS) and cathepsin B also reversed chlamydial killing.

178 the chlamydial inclusion and, thus, support chlamydial lipid acquisition and chlamydial development.

179 e chlamydial inclusion and are important for chlamydial lipid acquisition.

180 Here, we report on the role of the chlamydial lipooligosaccharide (LOS) in evading the immu

181 eficiency resulted in an increased amount of chlamydial lipopolysaccharide (LPS) within Chlamydia inc

182 hich was validated by directly measuring the chlamydial live organisms and genomes in the same organs

183 Chlamydial LOS was also a poor stimulator of maturation

184 Taken together, these data suggest that chlamydial LOS, which is remarkably conserved across the

185 ng pathways are not required for controlling chlamydial lower genital infection.

186 mproved management of diagnosed cases and of chlamydial morbidity, such as pelvic inflammatory diseas

187 dia mutant to induce hydrosalpinx, while the chlamydial mutant infection in the genital tract alone w

188 First, chlamydial mutants that are attenuated in inducing hydro

189 omolecular resolution and find support for a chlamydial needle-tip protein.

190 emonstrated the in vivo functionality of the chlamydial Opp transporter in C. trachomatis Importantly

191 pp transporter and determined that all three chlamydial OppA subunits supported oligopeptide transpor

192 Complementation of a CPAF-deficient chlamydial organism with a plasmid-encoded CPAF has enab

193 In a Chlamydia muridarum-C57 mouse model, chlamydial organisms are cleared from the genital tract

194 However, it remains unclear whether the chlamydial organisms can be introduced into the gastroin

195 a rapid but transient invasion of oviduct by chlamydial organisms can prevent the development of the

196 However, chlamydial organisms depleted of plasmid or deficient in

197 lation and confirmed the rapid ascent of the chlamydial organisms from the lower to upper genital tra

198 achomatis is a human genital tract pathogen, chlamydial organisms have frequently been detected in bo

199 Simultaneous monitoring of chlamydial organisms in individual organs or tissues rev

200 tant spreading led to stable colonization of chlamydial organisms in the colon.

201 we have demonstrated that the genital tract chlamydial organisms may use a systemic route to spread

202 gastrointestinal tract, suggesting that the chlamydial organisms may use the sexual behavior-indepen

203 The live chlamydial organisms recovered from rectal swabs reached

204 nt infection or inability of the plasmidless chlamydial organisms to trigger pathological responses,

205 We found that the gastrointestinal chlamydial organisms were cleared from the small intesti

206 Following an intravaginal inoculation, live chlamydial organisms were detected in mouse rectal swabs

207 Similar levels of live chlamydial organisms were recovered from oviduct tissues

208 host organelle recruitment between the three chlamydial organisms, with Simkania inclusions being tig

209 rves were being depleted by an intracellular chlamydial pathogen.

210 ion for both understanding the mechanisms of chlamydial pathogenesis and developing novel therapeutic

211 uch as time of day of chlamydia infection on chlamydial pathogenesis has not been determined.

212 for chlamydial growth in vitro, its role in chlamydial pathogenesis is clearly demonstrated in the g

213 n certain microbial infectivity, its role in chlamydial pathogenesis is unknown.

214 that the time of day of infection influences chlamydial pathogenesis, it indicates a possible associa

215 of gastrointestinal C. trachomatis in human chlamydial pathogenesis.

216 es, indicating a significant role of Pgp3 in chlamydial pathogenesis.

217 doptive transfers of CD8(+) T cells to study chlamydial pathogenesis.

218 encourage continued investigation of CPAF in chlamydial pathogenesis.

219 understanding this important contributor to chlamydial pathogenesis.

220 which may lead to a better understanding of chlamydial pathogenesis.

221 laid a foundation for further revealing the chlamydial pathogenic mechanisms.

222 irection/dimension for further investigating chlamydial pathogenic mechanisms.

223 investigation of the molecular mechanisms of chlamydial pathogenicity and development of medical util

224 Thus, chlamydial pathogenicity can be mediated by distinct hos

225 D8(+) T cells are sufficient for attenuating chlamydial pathogenicity in CD8 knockout mice.

226 th promoted chlamydial infection and reduced chlamydial pathogenicity in CD8(+) T cell-deficient mice

227 tract, we evaluated the effect of FTY720 on chlamydial pathogenicity in the current study.

228 onization of the gastrointestinal tract with chlamydial pathogenicity in the upper genital tract sugg

229 g that Pgp3m can be targeted for attenuating chlamydial pathogenicity or developed for blocking LL-37

230 correlation was more consistent than that of chlamydial pathogenicity with ascending infection in the

231 stigate the mechanisms of the CPAF-dependent chlamydial pathogenicity.

232 indicating a critical role of the plasmid in chlamydial pathogenicity.

233 -independent immune mechanism for regulating chlamydial pathogenicity.

234 lso found that OT1 mice can actively inhibit chlamydial pathogenicity.

235 that CD8(+) T cells are necessary to inhibit chlamydial pathogenicity.

236 e mechanisms by which CD4(+) T cells promote chlamydial pathogenicity.

237 itical role of Chlamydia-specific T cells in chlamydial pathogenicity.

238 ce), while others may directly contribute to chlamydial pathogenicity.

239 During infection chlamydial pathogens form an intracellular membrane-boun

240 epithelial cell class I- and class II-bound chlamydial peptides overlapped with peptides presented b

241 CD4(+) T cells but not CD8(+) T cells showed chlamydial persistence in the small intestine, indicatin

242 oping Chlamydia-specific Th1 immunity showed chlamydial persistence in the small intestine.

243 Chlamydial persistence is characterized by a halt in the

244 These results reveal the composition of chlamydial PG and disprove the "glycanless peptidoglycan

245 used a novel approach to metabolically label chlamydial PG using d-amino acid dipeptide probes and cl

246 picillin are consistent with the presence of chlamydial PG-modifying enzymes.

247 ed persistence, although profound changes in chlamydial physiology and gene expression occur in the p

248 molecular dissection of the function of the chlamydial plasmid and its individual genes or coding se

249 ts provide new insights into the role of the chlamydial plasmid as a chlamydial virulence factor and

250 , rather than the presence or absence of the chlamydial plasmid in the primary infecting strain, appe

251 with trachoma organisms lacking the cryptic chlamydial plasmid is highly attenuated in macaque eyes,

252 Our findings suggest that the chlamydial plasmid plays a focal role in the host cell i

253 ty and development of medical utility of the chlamydial plasmid system.

254 However, the chlamydial plasmid, which is essential for the induction

255 Current chlamydial plasmids are amalgamations of at least one an

256 t upon both the composition of the infecting chlamydial population and the genotype of the host, alon

257 d that the relative degree of virulence of a chlamydial population dictates the microRNA (miRNA) expr

258 ctor responsible for this suppression as the chlamydial protease- or proteasome-like activity factor,

259 CPAF (chlamydial protease-like activity factor), a Chlamydia s

260 extensive in vitro characterization of CPAF (chlamydial protease/proteasome-like activity factor), it

261 n was mediated through tyrosine nitration of chlamydial protein by peroxynitrite, an NO metabolite.

262 present epitopes from a limited spectrum of chlamydial proteins recognized by Chlamydia-specific CD4

263 rove useful to assess the secretion of other chlamydial proteins that are potentially exposed to the

264 A pivotal claim is that it was chlamydial proteins themselves that converted otherwise

265 Bioinformatic analyses of the chlamydial proteome also support the futalosine pathway

266 stive that TLR3 deficiency leads to enhanced chlamydial replication and possibly increased genital tr

267 In contrast, the inhibition of the chlamydial respiratory chain at mid-stage of the infecti

268 To investigate the chlamydial response mechanisms acting when other amino a

269 own that late genes transcribed by the major chlamydial RNA polymerase, sigma(66) RNA polymerase, are

270 transcribed from its own operon by the major chlamydial RNA polymerase.

271 . trachomatis Importantly, we found that one chlamydial SBP, OppA3 (Ct) , possessed dual substrate re

272 data suggest that genetic associations with chlamydial scarring disease may be focussed on processes

273 vealed that the long-lasting presence of the chlamydial signal was restricted to the gastrointestinal

274 terial organism that is related to classical chlamydial species and has been implicated as a cause of

275 Pathogenic chlamydial species are known to activate nucleotide-bind

276 ntibiotics, yet attempts to detect PG in any chlamydial species have proven unsuccessful (the 'chlamy

277 indicates that C. gallinacea is the endemic chlamydial species in chickens, whereas C. psittaci domi

278 y and are the strongest evidence so far that chlamydial species possess functional PG.

279 react only with antisera against the cognate chlamydial species.

280 ying and sequencing bacterial 16S as well as Chlamydiales-specific DNA.

281 have demonstrated that, following a delay in chlamydial spreading caused by FTY720, genital Chlamydia

282 The significance of the chlamydial spreading from the genital to GI tracts is di

283 However, FTY720 failed to block chlamydial spreading to the gastrointestinal tract.

284 shedding of live organisms, accelerated the chlamydial spreading to the GI tract.

285 evealed a potential intestinal resistance to chlamydial spreading.

286 roduced significantly reduced cytokines upon chlamydial stimulation, suggesting that reduced macropha

287 find striking similarities to the unrelated Chlamydiales, suggesting convergent adaptation to an obl

288 To understand how chlamydial supercoiling levels are regulated, we purifie

289 further correlated with a rapid decrease in chlamydial survival in the lower genital tract and reduc

290 The CPAF-dependent chlamydial survival in the lower genital tract was confi

291 as been much more extensively studied in the Chlamydiales than the Rickettsiales.

292 A chlamydial transposon insertion mutant in the Cdu1-encod

293 men reveal protective responses and identify chlamydial vaccine candidate antigens.

294 on is crucial to development of an effective chlamydial vaccine.

295 s is fundamental to designing an efficacious chlamydial vaccine.

296 otein-protein interactions that occur at the chlamydial vacuolar, or inclusion, membrane.

297 into the role of the chlamydial plasmid as a chlamydial virulence factor and its contributions to tra

298 ollectively, our results show that PmpD is a chlamydial virulence factor that functions in early host

299 tors; Pgp4 as a transcriptional regulator of chlamydial virulence-associated gene expression; and Pgp

300 sm has arisen as an essential contributor to chlamydial virulence.

301 Bacteria comprising the Chlamydiales were thought to be one of the few exception