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 Chlamydial Ags are subsequently generated through routes

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

6 tal of 4,316 samples were evaluated, and 281 chlamydial and 69 gonococcal infections were identified.

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

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

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

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

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

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

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

14 onse to ex vivo stimulation with inactivated chlamydial antigen secreted significantly more interleuk

15 Thus, we have identified chlamydial antigens and epitopes that are associated wit

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

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

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

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

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

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

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

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

24 Conjunctival infection with non-chlamydial bacteria may play an important role in the pr

25 te our understanding of the roles of CPAF in chlamydial biology and pathogenesis.

26 uttle vectors as genetic tools to understand chlamydial biology and pathogenicity as well as to devel

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

28 hose from control mice, despite an increased chlamydial burden.

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

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

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

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

33 s well as control mice, overcoming increased chlamydial colonization and tissue burden early during i

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

35 Correlation of chlamydial colonization of the gastrointestinal tract wi

36 ce displayed delayed clearance and increased chlamydial colonization.

37 w strategies for treatment and prevention of chlamydial complications.

38 recently proposed as the pathogenic basis of chlamydial complications.

39 protection because of the possibility that a chlamydial component drives a deleterious anamnestic T c

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

41 More effective chlamydial control measures are needed, but progress tow

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

43 Most importantly, in chlamydial culture, inhibition of CPAF with a specific i

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

45 orrelated with development and required both chlamydial de novo protein synthesis and T3SS activity.

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

47 amydial inclusion, no difference was seen in chlamydial development during infection of cells derived

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

49 We found chlamydial development to be inhibited in a dose-depende

50 us, support chlamydial lipid acquisition and chlamydial development.

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

52 hanges in DNA supercoiling levels during the chlamydial developmental cycle have been proposed as a g

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

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

55 is second subset represents a novel class of chlamydial developmental genes with features of both ear

56 ant women aged 19-45 years with a urogenital chlamydial diagnosis or a sexual partner with chlamydia

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

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

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

60 cestor of malaria parasites once contained a chlamydial endosymbiont.

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

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

63 re treated with doxycycline and assessed for chlamydial eradication and lymphoma response (primary en

64 and/or blood samples and were evaluable for chlamydial eradication, which was achieved in 14 patient

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

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

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

68 ral repressor that negatively regulates late chlamydial genes and prevents their premature expression

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

70 Expression of late chlamydial genes is upregulated during conversion from t

71 n severely hampered by the lack of a tenable chlamydial genetic system.

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

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

74 All chlamydial genomes contain the coding capacity for a non

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

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

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

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

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

80 the invasion of host cells but did result in chlamydial growth that closely mirrored that detected in

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

82 pithelial cells is blocked during productive chlamydial growth, thereby protecting chlamydiae from ba

83 and activity in infected cells and inhibited chlamydial growth.

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

85 why the macrophage environment is hostile to chlamydial growth.

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

87 Induction of chlamydial heat shock gene expression by elevated temper

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

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

90 Transcription of chlamydial heat shock genes is controlled by the stress

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

92 pulation that functions in antibody-mediated chlamydial immunity.

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

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

95 that syntaxin 6 and VAMP4 colocalize to the chlamydial inclusion and interact at the chlamydial incl

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

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

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

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

100 Although Panx1 was shown to localize to the chlamydial inclusion, no difference was seen in chlamydi

101 To investigate the role of syntaxin 6 at the chlamydial inclusion, we examined the localization and f

102 and is stabilized by deubiquitination at the chlamydial inclusion.

103 rans-Golgi SNARE syntaxin 6 localizes to the chlamydial inclusion.

104 ssociated membrane protein 4 (VAMP4), at the chlamydial inclusion.

105 of VAMP4, syntaxin 6 is not retained at the chlamydial inclusion.

106 the chlamydial inclusion and interact at the chlamydial inclusion.

107 Chlamydial inclusions are uncoupled from the endolysosom

108 During maturation of infected DCs, chlamydial inclusions disintegrate, likely because they

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

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

111 Chlamydial induction of EMT resulted in the generation o

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

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

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

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

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

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

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

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

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

121 with current, laboratory confirmed, genital chlamydial infection (n = 98) and one group of individua

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

123 rams have had remarkable success at reducing chlamydial infection and clinical signs of trachoma.

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

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

126 innate resistance protein in the control of chlamydial infection and may help explain why the macrop

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

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

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

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

131 processing occurred inside live cells during chlamydial infection and was not due to proteolysis duri

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

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

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

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

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

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

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

139 An RNA-based test detected ocular chlamydial infection in more children than did a DNA-bas

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

141 ow-derived DC line, we show that DCs control chlamydial infection in multiple small inclusions charac

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

143 Chlamydial infection in the lower genital tract can lead

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

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

146 eater understanding of the seroprevalence of chlamydial infection in US populations.

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

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

149 We previously showed that chlamydial infection increases markers of autophagy, an

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

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

152 Chlamydial infection was detected in the glandular epith

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

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

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

156 regulate chlamydial infection: one supports chlamydial infection, while the other plays a defensive

157 antly to oviduct pathology following genital chlamydial infection.

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

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

160 allmark of tubal infertility associated with chlamydial infection.

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

162 nses previously described for persistence of chlamydial infection.

163 lammasome-activation pathways during genital chlamydial infection.

164 for ASC in adaptive immunity during genital chlamydial infection.

165 elopment of oviduct pathology during genital chlamydial infection.

166 appear sensitive for the detection of ocular chlamydial infection.

167 may preferentially expose females to ocular chlamydial infection.

168 s administered to wild-type (WT) mice during chlamydial infection.

169 blasts and production of ECM proteins during chlamydial infection.

170 significant role for antibody in immunity to chlamydial infection.

171 of vATPase-bearing organelles that regulate chlamydial infection: one supports chlamydial infection,

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

173 rogression of Chlamydia infections, and with chlamydial infections at record levels in the US, we the

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

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

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

177 es against trachoma and sexually transmitted chlamydial infections.

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

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

180 4/CTL0063 is a virulence protein involved in chlamydial invasion.

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

182 intracellular bacteria comprising the order Chlamydiales lack the ability to synthesize nucleotides

183 gesting that PG synthesis is crucial for the chlamydial life cycle.

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

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

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

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

188 uctural and functional similarities with the chlamydial major outer membrane protein (MOMP), a strong

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

190 Drug treatment induced an aberrant chlamydial morphology consistent with persistent bodies.

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

192 exemplified by proposed similarity between a chlamydial ORFan protein and bacterial colicin pore-form

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

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 Simultaneous monitoring of chlamydial organisms in individual organs or tissues rev

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

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

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

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

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

204 an be used to express nonchlamydial genes in chlamydial organisms.

205 d the recruitment of a debranching enzyme of chlamydial pathogen origin.

206 rves were being depleted by an intracellular chlamydial pathogen.

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

208 ides the basis for understanding its role in chlamydial pathogenesis and serves as the platform for i

209 ortant information for further understanding chlamydial pathogenesis and the development of subunit v

210 gy, which will help us to further understand chlamydial pathogenesis and to develop anti-Chlamydia su

211 ions for understanding the plasmid's role in chlamydial pathogenesis at the molecular level.

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 erved ATP synthase, and it may contribute to chlamydial pathogenesis via mechanisms similar to those

215 encourage continued investigation of CPAF in chlamydial pathogenesis.

216 understanding this important contributor to chlamydial pathogenesis.

217 optotic tissue destruction may contribute to chlamydial pathogenesis.

218 of gastrointestinal C. trachomatis in human chlamydial pathogenesis.

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

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

221 um transformation system for further mapping chlamydial pathogenic and protective determinants in ani

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

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

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

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

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

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

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

229 During infection chlamydial pathogens form an intracellular membrane-boun

230 osol of effector proteins from intracellular Chlamydiales pathogens that allowed the host to utilize

231 osol of effector proteins from intracellular Chlamydiales pathogens.

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

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

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

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

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

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

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

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

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

241 The chlamydial plasmid plays an important role in the pathop

242 have provided information for further use of chlamydial plasmid shuttle vectors as genetic tools to u

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

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

245 serovar L2 organisms can be transformed with chlamydial plasmid-based shuttle vectors pGFP::SW2 and p

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

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

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

249 red cytosolic export of the virulence factor chlamydial protease-like activity factor, and interactio

250 sions disintegrate, likely because they lack chlamydial protease-like activity factor-mediated protec

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

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

253 A chlamydial protein called Tarp has been shown to nucleat

254 clusion was shown to be dependent on de novo chlamydial protein synthesis, but unlike syntaxin 6, VAM

255 rocessed and presented by HLA-B27 from three chlamydial proteins for which T-cell epitopes were predi

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

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

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

259 mydia trachomatis should greatly advance the chlamydial research.

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

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

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

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

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

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

266 Pathogenic chlamydial species are known to activate nucleotide-bind

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

268 In addition, expression of each chlamydial species IhtA rescued the lethal phenotype of

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

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

271 ibody reactivity with organisms of different chlamydial species, no statistically significant differe

272 A is a conserved mechanism across pathogenic chlamydial species, we cloned hctA and ihtA from C. trac

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

274 ing RNA (siRNA) knockdown of VAMP4 inhibited chlamydial sphingomyelin acquisition, correlating with a

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

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

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

278 primates demonstrates that plasmid-deficient chlamydial strains function as live attenuated vaccines

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

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

281 dent early genes is upregulated by increased chlamydial supercoiling levels in midcycle via their sup

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

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

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

285 Despite the importance of TLR2, major chlamydial TLR2 antigens have not been identified so far

286 A chlamydial transposon insertion mutant in the Cdu1-encod

287 CopN is a chlamydial type three secretion effector that is essenti

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

289 indicate that exposure to a live attenuated chlamydial vaccine or repeated abbreviated genital infec

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

291 s is fundamental to designing an efficacious chlamydial vaccine.

292 thogenicity as well as to develop attenuated chlamydial vaccines.

293 The chlamydial vacuole does not fuse with the defense cell o

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

295 as a novel authentic target for the putative chlamydial virulence factor CPAF, which should facilitat

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

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

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

299 hase gene glgA, that are likely important in chlamydial virulence.

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