ライフサイエンスコーパス: Chlamydia

1 l chemoattractant, is actively suppressed by Chlamydia.

2 es to gene regulation and stress response in Chlamydia.

3 gonorrhoea and 15 (12%) were diagnosed with chlamydia.

4 l other bacteria, indicating selectivity for Chlamydia.

5 iagnosed among 1427 (48%) participants (1434 chlamydia, 1242 gonorrhea, 252 syphilis).

6 were syphilis (6574), gonorrhea (64 995), or chlamydia (140 034).

7 lled out a questionnaire and were tested for chlamydia (2016-2017).

8 after syphilis (177.3), gonorrhea (73.2), or chlamydia (35.4) compared to women with no STI (22.4).

9 l (18/162), and 7.5% oropharyngeal (15/201); chlamydia, 5.0% urogenital (10/201), 11.7% rectal (19/16

10 n=18/162), and 7.5% oropharyngeal(n=15/201); chlamydia: 5.0% urogenital(n=10/201), 11.7% rectal(n=19/

11 usted IRR, 1.12 [95% CI, 1.02-1.23]) and for chlamydia (adjusted IRR, 1.17 [95% CI, 1.04-1.33]).

12 Chlamydia also causes long-term sequelae, but the role o

13 Chlamydia also upregulates transforming growth factor be

14 d a 15.2-fold higher unadjusted incidence of chlamydia and 34.9-fold higher unadjusted incidence of g

15 for 9.5% of the VHA population but 66.9% of chlamydia and 42.9% of gonorrhea cases.

16 es has implications for delayed clearance of Chlamydia and design of a Chlamydia vaccine.

17 chlamydia and gonorrhea infection, trends in chlamydia and gonorrhea in the Veterans Health Administr

18 Chlamydia and gonorrhea incidence rates in persons with

19 Chlamydia and gonorrhea incidence rates were calculated

20 y military servicemembers have high rates of chlamydia and gonorrhea infection, trends in chlamydia a

21 In 2019, testing for chlamydia and gonorrhea occurred in 2.3% of patients, 22

22 The incidence of chlamydia and gonorrhea rose dramatically from 2009-2019

23 VHA-wide adherence to chlamydia and gonorrhea testing in high-risk groups meri

24 2019 incidence of chlamydia and gonorrhea was 100.8 and 56.3 cases per 100

25 Tests and cases of chlamydia and gonorrhea were defined based on lab result

26 potential for studying cellular responses to Chlamydia and other sexually transmitted pathogens.

27 velopment of p.o. subunit vaccines to target Chlamydia and possibly other sexually transmitted pathog

28 our understanding of the natural history of chlamydia and the pathways through which prevention stra

29 r intestinal parasites, syphilis, gonorrhea, chlamydia, and human immunodeficiency virus, as well as

30 tions (STIs), including gonorrhea, syphilis, chlamydia, and trichomoniasis, is increasing by over 1 m

31 ctions (STIs) including gonorrhea, syphilis, chlamydia, and trichomoniasis, is increasing by over 1 m

32 Point-of-care testing (POCT) assays for chlamydia are being developed.

33 Antigen-specific CD4(+) T cells against Chlamydia are crucial for driving bacterial clearance an

34 Gonorrhea and chlamydia are important causes of pelvic inflammatory di

35 nfluence on behavior and disease risk, using chlamydia as a case study.

36 is well suited as a vaccine platform against chlamydia, as it is relatively affordable and scalable,

37 gh POCT sensitivity was needed to reduce the chlamydia-associated burden.

38 STI screening for syphilis AND gonorrhea/chlamydia at all anatomic sites and positivity at PrEP v

39 STI screening (syphilis and gonorrhea/chlamydia at all anatomic sites) and positivity at PrEP

40 reened biannually for syphilis and gonorrhea/chlamydia at all anatomic sites.

41 reened biannually for syphilis and gonorrhea/chlamydia at all anatomic sites.

42 % had a diagnosis of gonorrhea, syphilis, or chlamydia at any visit.

43 nts, of whom 319 had both rectal and vaginal chlamydia at enrollment, 22 had rectal chlamydia only, a

44 POCT on chlamydia prevalence, incidence, and chlamydia-attributable pelvic inflammatory disease (PID)

45 Chlamydia bacteria are obligate intracellular pathogens

46 Chlamydia binds several receptor tyrosine kinases (RTKs)

47 ple human pathogens, including Helicobacter, Chlamydia, Brucella, and Campylobacter.

48 easing screening coverage, reductions in the chlamydia burden could be realized with a POCT sensitivi

49 ia in vivo, resulting in significantly lower Chlamydia burden in the FRT and Chlamydia transport to t

50 of classical chlamydial antigens compromises Chlamydia (C.) pneumoniae serology.

51 horizontal and the vertical transmission of Chlamydia can be studied.

52 , the only known iron-dependent regulator in Chlamydia, can bind to the trpRBA intergenic region upst

53 with the numbers of syphilis, gonorrhea, and chlamydia cases (spearman coefficients 1.00, 0.94, and 0

54 sed bacterial burden in the FRT, accelerated Chlamydia clearance, and reduced hydrosalpinx pathology.

55 rizontal and vertical sexual transmission of Chlamydia closely parallels C. trachomatis sexual transm

56 ved effective against gonorrhea in gonorrhea/chlamydia-coinfected mice.

57 thral swabs and in the presence of simulated Chlamydia coinfection.

58 igher incidence rate than both gonorrhea and chlamydia combined.

59 oreover, p.o. immunization or infection with Chlamydia confers protection against per-vaginal (p.v.)

60 Although chlamydia (CT) and gonorrhea (GC) infections are increas

61 Although chlamydia (CT) and gonorrhea (GC) infections are increas

62 The sexually transmitted infections (STIs) chlamydia (CT) and gonorrhea (NG) are often asymptomatic

63 tified 26 class I-bound and 4 class II-bound Chlamydia-derived peptides from infected epithelial cell

64 lasses were identified: class 1 (n = 488; 9% chlamydia diagnosis) and class 2 (n = 325; 13% chlamydia

65 lamydia diagnosis) and class 2 (n = 325; 13% chlamydia diagnosis).

66 sk classes using psychological predictors of chlamydia diagnosis.

67 of TLR3 signaling in the immune response to Chlamydia Disruption of TLR3 function in these cells sig

68 FTY720 was recently reported to inhibit Chlamydia dissemination.

69 uctive tract (FRT) mucosa, it halts systemic Chlamydia dissemination.

70 Here, using chlamydia DNA as a clinically relevant target and high-t

71 g first diagnosis of syphilis, gonorrhea, or chlamydia during 2000-2015.

72 Chlamydia encodes homologs to proteins in the Rsb phosph

73 component of filopodia that are hijacked by Chlamydia entry.

74 Many intracellular bacteria, including Chlamydia, establish a parasitic membrane-bound organell

75 n C. trachomatis These findings suggest that Chlamydia evolved an oligopeptide transporter to facilit

76 Finally, the coinoculated gastrointestinal Chlamydia failed to directly spread to the genital tract

77 However, to our surprise, plasmid-deficient Chlamydia failed to produce infectious progenies in smal

78 the FTY720-resistant pathway(s) explored by Chlamydia for spreading to the gastrointestinal tract ma

79 Chlamydia frequently coexists with and exacerbates gonor

80 d donor mice were sufficient for eliminating Chlamydia from the small intestine but not the large int

81 a critical role for Th1 immunity in clearing Chlamydia from the small intestine but not the large int

82 genous IFN-gamma was sufficient for clearing Chlamydia from the small intestine but not the large int

83 critical role for CD4(+) T cells in clearing Chlamydia from the small intestine.

84 Newly developed tools for Chlamydia genetic manipulation have allowed us to genera

85 The T-cell response to chlamydia genital tract infections in humans and mice is

86 us may represent persistent infection, since Chlamydia genomes proliferated in the same tissues.

87 The primary outcome was incidence of chlamydia, gonorrhea, or syphilis.

88 olving to obligate intracellular dependence, Chlamydia has significantly reduced its genome size and

89 nce, and to date no vaccines against genital chlamydia have been tested in clinical trials.

90 her Incs bind eukaryotic proteins to promote chlamydia-host interactions.

91 lone was remarkably proficient at preventing chlamydia immunopathology, whereas the multifunctional T

92 rated a significant role of gastrointestinal Chlamydia in promoting pathology in the genital tract po

93 retions of p.o.-immunized animals neutralize Chlamydia in vivo, resulting in significantly lower Chla

94 ycin for the treatment of rectal and vaginal chlamydia in women.

95 f chlamydial lipopolysaccharide (LPS) within Chlamydia inclusions, which is suggestive that TLR3 defi

96 the induction of significant hydrosalpinx by Chlamydia, indicating that CD8(+) T cells are necessary

97 ombospondin-1 (Tsp1)-based peptide inhibited chlamydia-induced EMT, revealing a major source of activ

98 er understand the mechanisms associated with Chlamydia-induced genital tract pathogenesis in humans,

99 In contrast, the Chlamydia-induced synthesis of CCL5, IL-29 (IFN-lambda1)

100 in these cells significantly diminished the Chlamydia-induced synthesis of several inflammation biom

101 We hypothesized that Chlamydia-infected DCs and epithelial cells present over

102 sible association between complications from chlamydia infection and host circadian clock, which may

103 Genital chlamydia infection in women causes complications such a

104 Interestingly, we saw that Chlamydia infection induced the production of biomarkers

105 Human genital Chlamydia infection is a major public health concern due

106 Chlamydia infection is known to block the induction of a

107 f antibodies in protection against a primary Chlamydia infection is unclear and was a focus of this w

108 Possible factors, such as time of day of chlamydia infection on chlamydial pathogenesis has not b

109 t dampens the host innate immune response to Chlamydia infection.

110 ibutions of caspase-1 and -11 during genital Chlamydia infection.

111 ology and decreased fertility rate following Chlamydia infection.

112 ihood of developing more severe disease from Chlamydia infection.

113 between host and bacterial metabolism during Chlamydia infection.

114 Furthermore, analysis of human chlamydia-infection data with bulk expression profiles f

115 les analysed individually identified 3% more chlamydia infections than pooled (99.3%, 96.0%; p=0.027)

116 ted via intranasal (i.n.) or per-oral (p.o.) Chlamydia inoculation and that unlike the female reprodu

117 Thus, via a novel mechanism, Chlamydia inserts TarP within focal adhesions to alter t

118 in) and how these contribute to overall host-chlamydia interactions at this unique membrane is lackin

119 lamydial spreading caused by FTY720, genital Chlamydia is able to both spread to the gastrointestinal

120 Thus, genital Chlamydia is able to launch a 2nd wave of spreading via

121 The obligate intracellular bacterium Chlamydia is known to colonize mouse colon for long peri

122 The genital pathogen Chlamydia is known to colonize the gastrointestinal trac

123 Chlamydia is the most common sexually transmitted bacter

124 srupted in this ECD model will have a higher Chlamydia load, more pathology and decreased fertility r

125 circadian rhythms disrupted (ECD) had higher Chlamydia loads, more tissue alterations or lesions, and

126 ed that the obligate intracellular bacterium Chlamydia maintains its long-lasting colonization in the

127 A serologic test for antibodies to chlamydia may be a useful tool for trachoma surveillance

128 described observations together suggest that Chlamydia may have acquired the plasmid-encoded pGP3 to

129 expression within the developmental cycle of Chlamydia may play a crucial role in eliciting a protect

130 ract lumen, suggesting that gastrointestinal Chlamydia may promote genital pathology via an indirect

131 ich is remarkably conserved across the genus Chlamydia, may act both directly and indirectly to allow

132 epithelial cells present overlapping sets of Chlamydia-MHC class II epitopes to link inductive and ef

133 it model in which the mouse gastrointestinal Chlamydia might induce the second hit to promote genital

134 e were inoculated in the meatus urethra with Chlamydia muridarum and they were caged with naive femal

135 Chlamydia trachomatis and Chlamydia muridarum are intracellular bacterial pathogen

136 Orally delivered Chlamydia muridarum can reach the colon and maintain a l

137 (LD) cycle were infected intravaginally with Chlamydia muridarum either at zeitgeber time 3, ZT3 and

138 acterial clearance or immunopathology during Chlamydia muridarum genital tract infections.

139 h as hydrosalpinx, which can be modeled with Chlamydia muridarum infection in mice.

140 es to oviduct pathology during mouse genital Chlamydia muridarum infection.

141 tal tract virulence factor, is essential for Chlamydia muridarum to colonize the mouse gastrointestin

142 n the mouse model of genital infection using Chlamydia muridarum, IL-1R signaling plays a critical ro

143 Chlamydia trachomatis serovar L2 and Chlamydia muridarum, which do not express FtsZ, undergo

144 In a Chlamydia muridarum-C57 mouse model, chlamydial organism

145 arized division of Chlamydia trachomatis and Chlamydia muridarum.

146 To successfully complete its life cycle, Chlamydia must evade both intracellular innate immune re

147 a wild-type Chlamydia rescued an attenuated Chlamydia mutant to induce hydrosalpinx, while the chlam

148 No effective vaccine exists for Chlamydia, nor are there biomarkers available that readi

149 ginal chlamydia at enrollment, 22 had rectal chlamydia only, and 75 had vaginal chlamydia only.

150 ad rectal chlamydia only, and 75 had vaginal chlamydia only.

151 x) and were more likely to test positive for chlamydia or gonorrhea (8.6% vs 4.7% of nonusers; P = .0

152 x) and were more likely to test positive for chlamydia or gonorrhea (8.6% vs. 4.7% of non-users; p=0.

153 tinal tract may promote our understanding of Chlamydia pathogenic mechanisms.

154 The prototypical Inc, called IncA, enhances Chlamydia pathogenicity by promoting the homotypic fusio

155 cterial sexually transmitted infections, and Chlamydia pneumoniae causes community-acquired respirato

156 During invasion of host cells, Chlamydia pneumoniae secretes the effector protein CPn06

157 was lower and syphilis and rectal gonorrhea/chlamydia positivity was higher.

158 characteristics might be necessary to reduce chlamydia prevalence most effectively.

159 mycin distribution leads to decreased ocular chlamydia prevalence over a short-term period.

160 a significantly greater reduction in ocular chlamydia prevalence than the World Health Organization-

161 In retrospective analysis, chlamydia prevalence was estimated to be almost twice th

162 Ocular chlamydia prevalence was significantly different across

163 In some regions with high levels of ocular chlamydia prevalence, additional azithromycin distributi

164 d States, we estimated the impact of POCT on chlamydia prevalence, incidence, and chlamydia-attributa

165 uency of azithromycin distribution on ocular chlamydia prevalence.

166 POCT could improve chlamydia prevention efforts if test performance charact

167 asses the gastric barrier, plasmid-deficient Chlamydia produced infectious progenies in small intesti

168 At the tissue level, plasmid-positive Chlamydia produced infectious progenies throughout gastr

169 The structure of tubulin-bound CopN, a Chlamydia protein that delays nucleation, suggests that

170 ic acid amplification test for gonorrhea and chlamydia, rapid plasma reagin for syphilis) conducted a

171 rates, respectively, and a 12% reduction in chlamydia rates (RR: 0.884, 95% CI 0.883-0.885; P < .001

172 s) analysis of STI (syphilis, gonorrhea, and chlamydia) rates before (2000-2012) and after (2013-2017

173 A murine Chlamydia readily spreads from the mouse genital tract t

174 medical significance of the gastrointestinal Chlamydia remains unclear.

175 intragastric coinoculation with a wild-type Chlamydia rescued an attenuated Chlamydia mutant to indu

176 genital, rectal, and oropharyngeal gonorrhea/chlamydia, respectively.

177 genital, rectal, and oropharyngeal gonorrhea/chlamydia, respectively.

178 to what degree Tarp function contributes to Chlamydia's ability to parasitize mammalian host cells.

179 e following an intravaginal inoculation with Chlamydia Since T cells in OT1 mice are engineered to re

180 Surprisingly, orally inoculated Chlamydia sp. deficient in only plasmid-encoded pGP3 was

181 However, the small intestinal pGP3-deficient Chlamydia sp. failed to reach the large intestine, expla

182 , explaining the lack of live pGP3-deficient Chlamydia sp. in rectal swabs following an oral inoculat

183 vived significantly better than plasmid-free Chlamydia sp. in small intestinal tissues.

184 ge intestine, suggesting that pGP3-deficient Chlamydia sp. might be able to activate an intestinal re

185 inoculation, suggesting that pGP3-deficient Chlamydia sp. might be prevented from spreading from the

186 vate an intestinal resistance for regulating Chlamydia sp. spreading.

187 bypasses the gastric barrier, pGP3-deficient Chlamydia sp. still failed to reach the large intestine,

188 estinal tissues revealed that pGP3-deficient Chlamydia sp. survived significantly better than plasmid

189 Interestingly, pGP3-deficient Chlamydia sp. was able to colonize the colon following a

190 , although similarly inoculated plasmid-free Chlamydia sp. was able to do so.

191 the same mouse small intestine, plasmid-free Chlamydia sp. was no longer able to spread to the large

192 Nevertheless, orally inoculated plasmid-free Chlamydia sp. was still able to colonize the gut.

193 number of cases of syphilis, gonorrhea, and chlamydia (spearman coefficients 0.85, 0.81, and 0.85, r

194 Interestingly, the mouse-adapted Chlamydia species C. muridarum can infect mice both by t

195 pectrum of chlamydial proteins recognized by Chlamydia-specific CD4 T cells from immune mice.

196 eported that a subset of unrestricted murine chlamydia-specific CD8 T cells had a cytokine polarizati

197 splenocytes showed our previously published chlamydia-specific CD8 T-cell clones are MHC class II re

198 ol and s.c.-s.c.-immunized animals developed Chlamydia-specific intestinal IgA yet failed to develop

199 Both p.o. and s.c. immunizations induced Chlamydia-specific serum IgA.

200 vations have demonstrated a critical role of Chlamydia-specific T cells in chlamydial pathogenicity.

201 Mice deficient in developing Chlamydia-specific Th1 immunity showed chlamydial persis

202 ELISA antigens are cross-reactive among all Chlamydia spp., but Cpn and Ctr peptide antigens react o

203 ng hyperimmune mouse sera against each of 11 Chlamydia spp., we confirm that commercial Cpn and Ctr E

204 Since genital Chlamydia spreading to the gastrointestinal tract correl

205 The consequence of Chlamydia-stabilized focal adhesions was restricted cell

206 0-fold less infectious than plasmid-positive Chlamydia, suggesting that (i) the noninfectious status

207 tion Surveys, case report data from national chlamydia surveillance, and survey data from the Youth R

208 norrhoea test for 97 (80%) men and the first chlamydia test for 104 (86%) men.

209 andard-of-care group received gonorrhoea and chlamydia testing (cOR 18.65, 9.78-35.54; p<0.0001; aOR

210 trategy to increase uptake of gonorrhoea and chlamydia testing among MSM.

211 vidual-level characteristics associated with chlamydia testing and combined this with local-level cen

212 gramme, men were offered free gonorrhoea and chlamydia testing and given the option of donating money

213 synthesise data from multiple sources, using chlamydia testing as our example.

214 -care group, men were offered gonorrhoea and chlamydia testing at the standard patient price of yen 1

215 , allowing us to identify LAs where observed chlamydia testing rates were lower or higher than expect

216 this study was uptake of dual gonorrhoea and chlamydia testing, which we compared using chi(2) test a

217 with men (MSM) rarely receive gonorrhoea and chlamydia testing.

218 colonization of intracolonically inoculated Chlamydia Thus, we have demonstrated that, following a d

219 tract virulence factors may be essential for Chlamydia to maintain long-lasting colonization in the c

220 on in the colon while the plasmid may enable Chlamydia to reach the colon by promoting evasion of gas

221 r screening adolescents and young adults for Chlamydia trachomatis (C. trachomatis) and Neisseria gon

222 Chlamydia trachomatis (CT) and Mycoplasma genitalium (MG

223 Rectal infections with Chlamydia trachomatis (CT) are prevalent in women visiti

224 The Chlamydia trachomatis (CT) bacterial load could have imp

225 cy, and infertility in women with a previous Chlamydia trachomatis (CT) diagnosis compared with women

226 UU) was detected in 25 (17.2%) participants, Chlamydia trachomatis (CT) in 13 (9.0%), Mycoplasma geni

227 n many districts and a considerable level of Chlamydia trachomatis (Ct) infection was evident.

228 screening for Neisseria gonorrhoeae (NG) and Chlamydia trachomatis (CT) infections in all men who hav

229 Rectal Chlamydia trachomatis (CT) is common among clinic-attend

230 Chlamydia trachomatis (Ct) is the leading cause of bacte

231 extragenital Neisseria gonorrhoeae (NG) and Chlamydia trachomatis (CT) so universal extragenital sam

232 extragenital Neisseria gonorrhoeae (NG) and Chlamydia trachomatis (CT).

233 Chlamydia trachomatis and Chlamydia muridarum are intrac

234 distinct steps in the polarized division of Chlamydia trachomatis and Chlamydia muridarum.

235 itive risk score had point-of-care tests for Chlamydia trachomatis and Neisseria gonorrhoea (nucleic

236 Chlamydia trachomatis and Neisseria gonorrhoeae are the

237 Chlamydia trachomatis and Neisseria gonorrhoeae cases re

238 00/8800 systems (Cobas) for the detection of Chlamydia trachomatis and Neisseria gonorrhoeae was esta

239 rs, how the obligate intracellular bacterium Chlamydia trachomatis arrives at a physiologically simil

240 Chlamydia trachomatis can cause reproductive morbidities

241 tidoglycan assembles at the pole of dividing Chlamydia trachomatis cells where daughter cell formatio

242 Chlamydia trachomatis forms inclusions that are decorate

243 The Chlamydia trachomatis genome encodes multiple bifunction

244 xiella burnetii, Listeria monocytogenes, and Chlamydia trachomatis have developed bipartite metabolis

245 ltidomain type III secreted effector used by Chlamydia trachomatis In aggregate, existing data sugges

246 The epidemiology of Chlamydia trachomatis in the Middle East and north Afric

247 obiota in a cohort of 149 women with genital Chlamydia trachomatis infection at baseline who were fol

248 point of care test for detecting urogenital Chlamydia trachomatis infection in nonpregnant women and

249 Reproductive tract pathology caused by Chlamydia trachomatis infection is an important global c

250 Chlamydia trachomatis infection of the female genital tr

251 Chlamydia trachomatis infection of the human fallopian t

252 ver, when LOS synthesis was inhibited during Chlamydia trachomatis infection, HeLa cells regained sus

253 Chlamydia trachomatis is a bacterial pathogen causing oc

254 Although Chlamydia trachomatis is a human genital tract pathogen,

255 Chlamydia trachomatis is an obligate intracellular bacte

256 Chlamydia trachomatis is an obligate intracellular patho

257 The genital tract pathogen Chlamydia trachomatis is frequently detected in the gast

258 ar (TF) is common, but ocular infection with Chlamydia trachomatis is not.

259 The trp operon of Chlamydia trachomatis is organized differently from othe

260 ween genital and ocular clinical isolates of Chlamydia trachomatis is that only the former express a

261 Chlamydia trachomatis is the leading cause of bacterial

262 The obligate intracellular pathogen Chlamydia trachomatis is the leading cause of noncongeni

263 Chlamydia trachomatis is the leading cause of sexually t

264 Chlamydia trachomatis is the most common sexually transm

265 Chlamydia trachomatis is the most common sexually transm

266 Chlamydia trachomatis is the most common sexually transm

267 Chlamydia trachomatis is the most commonly reported bact

268 In some women, sexually transmitted Chlamydia trachomatis may ascend to infect the endometri

269 Sexually transmitted infection with Chlamydia trachomatis may lead to fibrotic blockage in w

270 er paper and dried to test for antibodies to Chlamydia trachomatis pgp3 using the Luminex platform.

271 ryngeal and rectal Neisseria gonorrhoeae and Chlamydia trachomatis play important roles in infection

272 Although the Chlamydia trachomatis protein Cta1 has been identified t

273 Chlamydia trachomatis serovar L2 and Chlamydia muridarum

274 The lack of resistance in Chlamydia trachomatis suggests that azithromycin might r

275 The human pathogen Chlamydia trachomatis targets epithelial cells lining th

276 cts of control strategies on the dynamics of Chlamydia trachomatis transmission are difficult to quan

277 Chlamydia trachomatis, a leading infectious cause of tub

278 ncluding the obligate intracellular pathogen Chlamydia trachomatis, grow within a membrane-bound bact

279 One such pathogen, Chlamydia trachomatis, has a limited capacity to synthes

280 dered idiopathic when Neisseria gonorrhoeae, Chlamydia trachomatis, Mycoplasma genitalium, Trichomona

281 Positivity rates for Chlamydia trachomatis, Neisseria gonorrhoeae, and Tricho

282 Specimens were tested for M. genitalium, Chlamydia trachomatis, Neisseria gonorrhoeae, Trichomona

283 m, P = .04; HSV-2, P = .001; and a trend for Chlamydia trachomatis, P = .06).

284 The obligate intracellular bacteria Chlamydia trachomatis, the causative agent of trachoma a

285 gnificantly reduces the prevalence of ocular Chlamydia trachomatis, the causative organism of trachom

286 seria gonorrhoeae, Streptococcus agalactiae, Chlamydia trachomatis, Trichomonas vaginalis, and Candid

287 e first, found in the intracellular pathogen Chlamydia trachomatis, uses YhhQ and tRNA guanine transg

288 ns with the obligate intracellular bacterium Chlamydia trachomatis, variation in immune activation an

289 llowing repeated conjunctival infection with Chlamydia trachomatis, which causes a chronic inflammato

290 t the major outer membrane protein (MOMP) of Chlamydia trachomatis.

291 ted with the obligate intracellular bacteria Chlamydia trachomatis.

292 ating Psychological Determinants: Control of Chlamydia Transmission (iMPaCT) Study) filled out a ques

293 cantly lower Chlamydia burden in the FRT and Chlamydia transport to the GIT.

294 Thus, RTK-mediated host invasion by chlamydia upregulated TGF-beta expression and signaling,

295 The results revealed that Chlamydia upregulated TGF-beta expression as early as 6

296 ty and immunogenicity, in humans, of a novel chlamydia vaccine based on a recombinant protein subunit

297 layed clearance of Chlamydia and design of a Chlamydia vaccine.

298 positivity for syphilis and rectal gonorrhea/chlamydia was higher.

299 innate immune components that interact with Chlamydia, we introduced C. trachomatis into mouse endom

300 Sexually transmitted Chlamydia, which can cause fibrotic pathology in women's