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1 C. trachomatis and T. vaginalis infection increase the s
2 C. trachomatis assembles its membrane systems from the u
3 C. trachomatis has adjacent genes encoding the separate
4 C. trachomatis multiplies exclusively inside host cells
5 C. trachomatis samples were typed using multilocus seque
6 C. trachomatis strains can be differentiated by sequenci
7 C. trachomatis was detected at follow-up in 39 subjects
8 C. trachomatis was detected from 59 rectal swabs and 8 p
10 (adjusted odds ratio [AOR], 1.75; P = .103), C. trachomatis (AOR, 1.43; P = .247), and T. vaginalis (
11 e, 37/45 C. trachomatis-positive and 197/212 C. trachomatis-negative samples were detected (sensitivi
13 1-7.1]), HSV-2 excretion (26.7 [2.9-244.3]), C. trachomatis (11.7 [2.3-58.9]), and M. genitalium infe
15 Using the plasmid-based assay alone, 37/45 C. trachomatis-positive and 197/212 C. trachomatis-negat
16 reated HLA-DR4 transgenic mice with 5 x 10(5)C. trachomatis D inclusion forming units (IFU) induced a
18 c manipulation have allowed us to generate a C. trachomatis strain expressing a heterologous CD4(+) T
26 5% confidence interval [CI], 9.5%-24.0%) and C. trachomatis prevalence was 14.7% (95% CI, 7.8%-21.6%)
27 (odds ratio [OR] 0.85, 95% CI 0.75-0.95) and C. trachomatis infection (OR 0.67, 95% CI 0.55-0.78).
29 tion testing would detect N. gonorrhoeae and C. trachomatis (or T. vaginalis if utilized), there is n
30 greement for detection of N. gonorrhoeae and C. trachomatis for 3 investigational assays compared to
31 greement for detection of N. gonorrhoeae and C. trachomatis for three investigational assays compared
33 1% in the pharynx and 7.9% in the rectum and C. trachomatis positivity of 2.0% in the pharynx and 8.7
34 using a novel cis complementation approach, C. trachomatis lacking tarP demonstrated significant att
35 ia species associated with human disease are C. trachomatis, which is the leading cause of both repor
36 DNA for whole-genome sequencing; however, as C. trachomatis is an obligate intracellular pathogen, th
37 mido thiazolino 2-pyridones which attenuated C. trachomatis infectivity without affecting host cell o
38 tes of the proportion of PID cases caused by C. trachomatis are 35% (95% credible interval [CrI], 11%
41 s in mammalian cells, themselves hijacked by C. trachomatis to sustain their own metabolic needs.
43 he NOD2-dependent activation of NF-kappaB by C. trachomatis-infected cell lysates as a biomarker for
44 utamate reduced in vivo synthesis of mDAP by C. trachomatis to undetectable levels, thus confirming t
45 hospholipid molecular species synthesized by C. trachomatis contained oleic acid, an abundant host fa
46 included 98 women who were contact-traced by C. trachomatis-positive sex partners at the STI outpatie
48 can be challenging, as mice naturally clear C. trachomatis when it is deposited in the lower genital
49 by comparison to a 6-month audit of clinical C. trachomatis TMA (12,999 specimens) on the basis of th
55 Cepheid Xpert CT/NG assay (Xpert) to detect C. trachomatis and N. gonorrhoeae in rectal and pharynge
57 eatment were new infections with a different C. trachomatis strain rather than reinfection with the s
59 orted more often in subjects with discordant C. trachomatis strains than in those with concordant str
61 277 samples from 260 MSM identified distinct C. trachomatis strains circulating concurrently over tim
62 This study investigates whether distinct C. trachomatis strains circulate among subpopulations wi
64 days, respectively) in two studies: (i) dry C. trachomatis-seeded swabs were used with ACT after sto
65 e report that levels of CXCL10 change during C. trachomatis infection of cultured cells in a manner d
67 g different urine samples spiked with either C. trachomatis or N. gonorrhoeae, and also containing bo
68 , reported recent sexual contact with either C. trachomatis or N. gonorrhoeae, or had symptoms of an
70 the fecal-oral route; (2) in the modern era, C. trachomatis causes "opportunistic" infection at non-G
74 survivin levels was also detected following C. trachomatis infection, which was reversed by blocking
77 [95% confidence interval {CI}, .20-1.23] for C. trachomatis infection, 0.56 [95% CI, .19-1.67] for N.
80 a, and conjunctival swabs were collected for C. trachomatis detection and to analyze the expression o
81 fferent chemokine receptors are critical for C. trachomatis-specific CD4(+) T cells to home to the lu
82 nstrate that FASII activity is essential for C. trachomatis proliferation within its eukaryotic host
84 n used to predict up to 59 putative Incs for C. trachomatis; however, localization to the inclusion m
87 p in 9 of 11 (82%) participants positive for C. trachomatis and 7 of 10 (70%) participants positive f
89 with highest diagnostic yield is rectum for C. trachomatis and rectum and oropharynx for N. gonorrho
90 polymerase chain reaction [PCR] results for C. trachomatis DNA by Roche Amplicor) and 25 true-negati
91 two methods did not differ significantly for C. trachomatis (P = 0.774) or N. gonorrhoeae (P = 0.163)
92 esulted in collection of 2,408 specimens for C. trachomatis, N. gonorrhoeae, and T. vaginalis TMA scr
94 y analyzed data from 655 patients tested for C. trachomatis (887 specimens) and N. gonorrhoeae (890 s
103 econd HLA-B27-restricted T-cell epitope from C. trachomatis with relevance in ReA demonstrated to be
104 scherichia coli was toxic to cells, LOS from C. trachomatis did not induce any appreciable cell death
105 periplasmic domain of the RsbU protein from C. trachomatis (PDB 6MAB) displays close structural simi
106 ia pseudotuberculosis and also secreted from C. trachomatis in infected cells where it localizes appr
109 s-mucosa protective immunity against genital C. trachomatis infection following intranasal immunizati
110 ositive predictive values for M. genitalium, C. trachomatis, N. gonorrhoeae, and T. vaginalis were 10
112 er, relatively little is known regarding how C. trachomatis is able to hijack host cell metabolism.
115 ice, which replicates many features of human C. trachomatis infection and avoids the characteristic l
117 (tri-diaminopimelic acid) in E. coli and in C. trachomatis These findings suggest that Chlamydia evo
123 e data point to an AasC-dependent pathway in C. trachomatis that selectively scavenges host saturated
128 evelopments in the genetic transformation in C. trachomatis, we constructed a versatile green fluores
129 onality of the chlamydial Opp transporter in C. trachomatis Importantly, we found that one chlamydial
130 C. trachomatis detection after treatment in C. trachomatis-infected subjects seen at a sexually tran
131 to demonstrate DapF (Ct) function in vivo in C. trachomatis We reasoned that, because DapF (Ct) utili
132 ne-bound intracellular niche, the inclusion, C. trachomatis relies on a set of effector proteins that
133 ignificantly reduced IFN-gamma and increased C. trachomatis burden in the endometrial tissue, confirm
136 tty acids were incorporated exclusively into C. trachomatis-produced phospholipid molecular species.
137 s added to the medium were incorporated into C. trachomatis-derived phospholipid molecular species.
138 that interact with Chlamydia, we introduced C. trachomatis into mouse endometrium via transcervical
139 uridarum, a model pathogen for investigating C. trachomatis pathogenesis, readily spreads from the mo
141 The exploitation of genetically labeled C. trachomatis organisms with P3-driven GFP allows for t
143 basis of bioinformatic analysis of multiple C. trachomatis genomes, led us to re-evaluate the previo
144 hus, we screened a population of mutagenized C. trachomatis strains for mutants that failed to reacti
147 report the whole-genome sequences of ocular C. trachomatis isolates obtained from young children wit
148 rethra/cervix) testing identified 92-100% of C. trachomatis or N. gonorrhoeae infections in participa
150 imilar large sample of data on the burden of C. trachomatis and N. gonorrhoeae infections by anatomic
151 P3 region verifies that P3 is a new class of C. trachomatis sigma(66)-dependent promoter, which requi
154 Ms support the full infectious life cycle of C. trachomatis in a manner that mimics the infection of
156 l specimens resulted in greater detection of C. trachomatis (6.1% and 11.3% rates, respectively) than
157 critical for the comprehensive detection of C. trachomatis and N. gonorrhoeae in the pediatric popul
158 identity factors may influence detection of C. trachomatis and N. gonorrhoeae infections at specific
160 he sensitivity of Cobas for the detection of C. trachomatis in female specimens was 95.6% (95% confid
161 city estimates of Cobas for the detection of C. trachomatis in male urine samples were 100% (96.8% to
163 egradation in the AC2 assay for detection of C. trachomatis or N. gonorrhoeae was observed, although
164 Probe Aptima Combo 2 assay) for detection of C. trachomatis ribosomal RNA (rRNA) from direct ocular s
166 ehaviors impact the anatomic distribution of C. trachomatis and N. gonorrhoeae infection is needed to
167 fection prevented the first cell division of C. trachomatis, although the cell morphology suggested d
168 ic review to investigate the epidemiology of C. trachomatis organism load in human genital chlamydia
169 ays a significant role in the eradication of C. trachomatis during the infection of macrophages.
170 ative PCR analysis showed that expression of C. trachomatis glycolytic enzymes inversely correlated w
171 esent in serum, rapidly induce expression of C. trachomatis tryptophan synthase, even under condition
172 oyl-acyl carrier protein reductase (FabI) of C. trachomatis to determine whether chlamydial FASII is
173 progress has been hindered by the failure of C. trachomatis to induce clinically relevant pathology i
175 our study displayed the clinical features of C. trachomatis and N. gonorrhoeae, the 2 organisms that
176 study the development-dependent function of C. trachomatis promoters in an attempt to elucidate the
178 e activity of DapF compromises the growth of C. trachomatis Thus, a substrate competition strategy ca
179 t several analogues can impair the growth of C. trachomatis without affecting host cell viability.
180 ld be protected by vaccination, 10(4) IFU of C. trachomatis D was delivered intranasally, and mice we
182 lls were infected with a clinical isolate of C. trachomatis, and inclusions containing chlamydial dev
183 mid-free lymphogranuloma venereum isolate of C. trachomatis, serovar L2, with either the original shu
185 d as few as 10 inclusion-forming units/ml of C. trachomatis in less than 9 min, including DNA extract
186 rs were also associated with reduced odds of C. trachomatis infection: lack of ocular discharge (OR 0
187 derivatives de-repress the trpRBA operon of C. trachomatis strains with trpA or trpB mutations, no a
189 with men, have shown that the prevalence of C. trachomatis and N. gonorrhoeae infections is much hig
191 ting, the estimated population prevalence of C. trachomatis ocular infection was approximately 17.5%.
194 have been associated with increased risk of C. trachomatis infection, suggesting that the impact of
196 Biochemical analysis established the role of C. trachomatis-encoded acyltransferases in producing the
197 tion of Cdu1 led to increased sensitivity of C. trachomatis for IFNgamma and impaired infection in mi
199 Due to the genetically intractable status of C. trachomatis at that time, this model of IncD-CERT int
201 ed that the putative OppABCDF transporter of C. trachomatis functions in both oligopeptide transport
205 d avoids the characteristic low virulence of C. trachomatis in the mouse, we previously demonstrated
206 conducted whole-genome sequence analysis on C. trachomatis isolates collected from a previously desc
209 ts with monoinfections with M. genitalium or C. trachomatis compared to women with no detectable STIs
210 to be significantly associated with TF/TI or C. trachomatis infection, and the use of sanitation faci
211 transmission of Chlamydia closely parallels C. trachomatis sexual transmission in humans and may be
214 strated a critical role of CPAF in promoting C. trachomatis survival in the mouse lower genital tract
217 ng of Inc function(s), we subjected putative C. trachomatis Incs to affinity purification-mass spectr
218 ormatics analysis suggests that the putative C. trachomatis oligopeptide transporter OppABCDF (OppABC
220 f anal intercourse, were screened for rectal C. trachomatis using the Gen-Probe Aptima COMBO 2 Assay.
221 revalence and factors associated with rectal C. trachomatis among female sexually transmitted infecti
223 Our study demonstrates that most repeat C. trachomatis detections after treatment were new infec
224 ng to investigate the epidemiology of repeat C. trachomatis detection after treatment in C. trachomat
228 ere we present the structure of the secreted C. trachomatis protein Pgp3, an immunodominant antigen a
230 fection, a model that has been used to study C. trachomatis pathogenesis in women, is known to depend
232 t within a few days, while a CPAF-sufficient C. trachomatis strain (L2-5) survived in the lower genit
233 Although several lines of evidence suggest C. trachomatis utilizes host phospholipids, the bacteriu
234 haracterized for 93 women, of whom 52 tested C. trachomatis positive and 41 C. trachomatis negative.
235 eless, C. muridarum Pgp5 is more potent than C. trachomatis Pgp5 in suppressing gene expression.
236 tions were significantly more prevalent than C. trachomatis and N. gonorrhoeae infections, while the
240 ogether with the intriguing observation that C. trachomatis CopN does not bind tubulin, our data supp
243 ry, this experimental approach revealed that C. trachomatis broadly alters host proteins and can be a
250 s lactate dehydrogenase, are enriched at the C. trachomatis inclusion membrane during infection.
251 s TMA (12,999 specimens) on the basis of the C. trachomatis detection rate, specimen source distribut
252 We previously proposed that insertion of the C. trachomatis effector protein IncD into the inclusion
253 a presented here show that expression of the C. trachomatis effector protein IncD mediates the recrui
255 ars; P < 0.0001) and higher than that of the C. trachomatis-infected females (mean, 23.8 years; P = 0
259 rtion of reproductive damage attributable to C. trachomatis Further studies using modern assays in co
262 lation excess fractions (PEFs) of PID due to C. trachomatis, using routine data, surveys, case-contro
264 of excess l-glutamate or meso-DAP (mDAP) to C. trachomatis resulted in 90% reduction in bacterial ti
265 roach to other host cytokines in response to C. trachomatis and found evidence that RANTES, another T
266 elected by evolution as the host response to C. trachomatis in the human female genital tract to cont
269 onses were associated with susceptibility to C. trachomatis, whereas cytokines involved in Th1 polari
270 for successful CD4(+) T cell trafficking to C. trachomatis-infected tissues, we will be better equip
271 and young adults for Chlamydia trachomatis (C. trachomatis) and Neisseria gonorrhoeae (N. gonorrhoea
274 eotide transporters, the ATP/ADP translocase C. trachomatis Npt1 (Npt1(Ct)) and the nucleotide unipor
277 nflammation- and caspase-inducing, wild-type C. trachomatis serovar L2 led to infertility, but the no
278 isolates appear to be recombinants with UGT C. trachomatis genome backbones, in which loci that enco
279 uridarum, a murine model of human urogenital C. trachomatis, with severely attenuated disease develop
280 igens that can be applied to humans, we used C. trachomatis serovar D (strain UW-3/Cx) to induce infe
283 d that CVM was significantly associated with C. trachomatis infection (odds ratio [OR], 4.2 [95% conf
287 with positive cultures) mice challenged with C. trachomatis serovars of the same complex were protect
288 from patients with symptoms consistent with C. trachomatis conjunctivitis and with previously demons
289 By comparison, mice vaginally infected with C. trachomatis exhibited transient low-burden infections
290 ling of human epithelial cells infected with C. trachomatis plasmid-bearing (A2497) and plasmid-defic
292 ical assays, we observed that infection with C. trachomatis led to downregulated expression of induci
293 re susceptible to endometrial infection with C. trachomatis, suggesting a role for group 3-like ILCs
296 ccinated by mucosal and systemic routes with C. trachomatis serovar D (UW-3/Cx) rMOMP and challenged
297 for up to 84 days and (ii) swabs seeded with C. trachomatis and N. gonorrhoeae and then placed in tra
299 ited symptomatic and asymptomatic women with C. trachomatis (CT) infection and asymptomatic, uninfect