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1 ns, and lower fertility rate associated with chlamydial infection.
2 al factor infertility resulting from genital chlamydial infection.
3 detection of trichomonal, gonococcal, and/or chlamydial infection.
4  response in the female genital tract during chlamydial infection.
5  TNF-alpha released in situ during secondary chlamydial infection.
6 rophils has important effects in vivo during chlamydial infection.
7 y end point was newly acquired gonococcal or chlamydial infection.
8 d to localize the endogenous proteins during chlamydial infection.
9 ve protective immunity against human genital chlamydial infection.
10 essure for maintaining pgp3 secretion during chlamydial infection.
11 y without affecting the host defense against chlamydial infection.
12 ng RNA failed to produce IL-8 in response to chlamydial infection.
13  its recommendations regarding screening for chlamydial infection.
14 not play a significant role in resolution of chlamydial infection.
15 r differential susceptibility against murine chlamydial infection.
16 hose with gonorrheal infection, 46% also had chlamydial infection.
17 y selected villages were assessed for ocular chlamydial infection.
18 ys in induction of IP-10 and IFN-beta during chlamydial infection.
19 ates of persistent or recurrent gonorrhea or chlamydial infection.
20 blasts and production of ECM proteins during chlamydial infection.
21 onse by nonimmune cells in host clearance of chlamydial infection.
22 te the host innate antimicrobial response to chlamydial infection.
23 s) in induction of IFN-beta and IP-10 during chlamydial infection.
24 hnicity, and HIV-1 infection did not predict chlamydial infection.
25 s both produced and immunogenic during human chlamydial infection.
26 ctivities have been reported to occur during chlamydial infection.
27 t-catch urines [FCU]) for diagnosing genital chlamydial infection.
28 teractions that may contribute to persistent chlamydial infection.
29 not protect against urogenital gonococcal or chlamydial infection.
30 (SE, 0.8%) is estimated to have an untreated chlamydial infection.
31 cient in their ability to sustain productive chlamydial infection.
32 ehavioural determinants of prevalent genital chlamydial infection.
33 he presence of symptoms were associated with chlamydial infection.
34 ollowed by selection for clones resistant to chlamydial infection.
35 ased Th1 response and a shorter, more benign chlamydial infection.
36 mmunotherapeutic vaccination against genital chlamydial infection.
37 n important cytokine in host defense against chlamydial infection.
38 cally in providing immunity in this model of chlamydial infection.
39 egulation of the susceptibility of mice to a chlamydial infection.
40 significant role for antibody in immunity to chlamydial infection.
41 e as a novel approach to vaccination against chlamydial infection.
42 infection, transmission, and the sequelae of chlamydial infection.
43 ly mimics the immune response produced after chlamydial infection.
44 cells, and adjacent to glands in response to chlamydial infection.
45 ment or function during primary or secondary chlamydial infection.
46 antly to oviduct pathology following genital chlamydial infection.
47  Yersinia spp., have an inhibitory effect on chlamydial infection.
48 fine the role of PmpD in the pathogenesis of chlamydial infection.
49 allmark of tubal infertility associated with chlamydial infection.
50 n between TGF-beta and EGFR signaling during chlamydial infection.
51 of DNA sensors in IFN-beta expression during chlamydial infection.
52 nses previously described for persistence of chlamydial infection.
53 lammasome-activation pathways during genital chlamydial infection.
54  for ASC in adaptive immunity during genital chlamydial infection.
55 elopment of oviduct pathology during genital chlamydial infection.
56 appear sensitive for the detection of ocular chlamydial infection.
57  may preferentially expose females to ocular chlamydial infection.
58 s administered to wild-type (WT) mice during chlamydial infection.
59  optimal oviduct pathology following genital chlamydial infection.
60 ed a Th1/Th17-dominant immune response after chlamydial infection.
61 t result for trichomonal, gonococcal, and/or chlamydial infection.
62 tics, and its laboratory correlates in human chlamydial infection.
63 n the genital tract during the first week of chlamydial infection.
64 s in innate and adaptive immune responses to chlamydial infection.
65 t for the establishment and maintenance of a chlamydial infection.
66 re is no FDA-approved treatment specific for chlamydial infections.
67  optimal protective immunity against genital chlamydial infections.
68 ost effective strategy for controlling human chlamydial infections.
69 ine or drug targets for the control of human chlamydial infections.
70 al significance to the pathogenesis of human chlamydial infections.
71 at apoptosis has an immunomodulatory role in chlamydial infections.
72 role in the inflammatory processes caused by chlamydial infections.
73 e an important factor in the pathogenesis of chlamydial infections.
74 fections, but not before they resolved their chlamydial infections.
75 e protective or pathological role of CTLs in chlamydial infections.
76 es against trachoma and sexually transmitted chlamydial infections.
77 ammatory disease versus 14.4% (5.9-24.6%) of chlamydial infections.
78 t vs. 11 percent, P=0.01) than in those with chlamydial infection (11 percent vs. 13 percent, P=0.17)
79 compared with those with upper genital tract chlamydial infection (13.8% vs 9.5%; P =04), but the CD4
80 ents had single infections (15 gonorrhea, 10 chlamydial infection, 3 trichomoniasis), and 4 had dual
81 (mostly *0602 and *0603) was associated with chlamydial infection (49% vs. 34%; adjusted relative odd
82            The estimated number of untreated chlamydial infections (5231; SE, 1395) is also greater t
83 han in the comparison condition had incident chlamydial infections (94 vs 104 participants, respectiv
84 for incident trichomonal, gonococcal, and/or chlamydial infection (adjusted hazard ratio [AHR] for in
85           qLCR will be useful for studies of chlamydial infection aimed at understanding the associat
86                             Risk factors for chlamydial infection among men aged 20 to 44 years were
87  study of the effectiveness of screening for chlamydial infection among nonpregnant women at increase
88                                      Current chlamydial infection among surgical cases was low (6%) a
89     To estimate the prevalence of urogenital chlamydial infection among young, low-income women in no
90 rams have had remarkable success at reducing chlamydial infection and clinical signs of trachoma.
91 ective effector and memory responses against chlamydial infection and demonstrates that an effective
92 ations on the epidemiology and management of chlamydial infection and disease in humans.
93 ng was associated with a lower prevalence of chlamydial infection and fewer reported cases of pelvic
94 97% when urine samples were tested, for both chlamydial infection and gonorrhea and in both men and w
95 e new information about the pathogenomics of chlamydial infection and insights for improving murine m
96  innate resistance protein in the control of chlamydial infection and may help explain why the macrop
97 roteasome-like activity factor), its role in chlamydial infection and pathogenesis remains unclear.
98 study, we evaluated the role of caspase-1 in chlamydial infection and pathogenesis.
99 cipants with a laboratory-confirmed incident chlamydial infection and percentage of participants with
100 ce depletion of CD4(+) T cells both promoted chlamydial infection and reduced chlamydial pathogenicit
101 ears to identify the subset of patients with chlamydial infection and significant CAD.
102                         Patients with rectal chlamydial infection and signs or symptoms of proctitis
103 es (MMPs) would be enhanced following murine chlamydial infection and that their expression would var
104 been implicated in susceptibility to genital chlamydial infection and the development of tubal pathol
105 ing of pulsed dendritic cells to the site of chlamydial infection and the induction of a local protec
106 processing occurred inside live cells during chlamydial infection and was not due to proteolysis duri
107  protein was detected as early as 12 h after chlamydial infection and was present in the inclusion me
108 ion of deleterious immune responses in human chlamydial infections and has been found to colocalize w
109 assessed, conjunctival swabs were tested for chlamydial infection, and blood spots were collected on
110 tween pathogenic and protective responses to chlamydial infection, and genes controlling NO productio
111 or chlamydia, to retest infected females for chlamydial infection, and to co-treat individuals with g
112 ast infection was negatively associated with chlamydial infection (AOR = 0.28; 95% CI = 0.10 to 0.83)
113 of a major category of altered miRNAs during chlamydial infection are key components of the pathophys
114 s for the diagnosis of rectal gonococcal and chlamydial infection are optimal.
115                              The sequelae of chlamydial infections are likely due to immunopathologic
116 d studies on the natural history of repeated chlamydial infections are needed.
117 ny sex partners of persons with gonorrhea or chlamydial infections are not treated, which leads to fr
118                              Moreover, acute chlamydial infections are often asymptomatic.
119 ed fifteen children were examined for ocular chlamydial infection at baseline.
120 be used to profile human immune responses to chlamydial infection at the whole-genome scale.
121 rogression of Chlamydia infections, and with chlamydial infections at record levels in the US, we the
122     Inhibition of MCP-1 is not beneficial in chlamydial infection because of its pleiotropic effects.
123  that female reproductive hormones influence chlamydial infection both in vivo and in vitro.
124 ction in the early phase of host response to chlamydial infection but also plays a critical role in t
125 n synthesis or trafficking in the absence of chlamydial infection but reduced the amount of sphingomy
126 udies assessed PID diagnosis after untreated chlamydial infection, but rates varied widely, making it
127                Inflammation is a hallmark of chlamydial infections, but how inflammatory cytokines ar
128 asmic reticulum nor inhibition of subsequent chlamydial infection by ectopically expressed proteins c
129 pecimens testing positive for gonococcal and chlamydial infection by ligase chain reaction, weighted
130 hat basal levels of ROS are generated during chlamydial infection by NADPH oxidase, but ROS levels, r
131 hildren and adults were monitored for ocular chlamydial infection by polymerase chain reaction.
132 ell physiology and thereby susceptibility to chlamydial infection by reverse-stage, exogenous hormona
133     A positive test result for gonococcal or chlamydial infection by the ligase chain reaction assay;
134 lyzed the frequency and predictors of repeat chlamydial infection by using a population-based chlamyd
135 se of sexually transmitted disease in women, chlamydial infections can lead to pelvic inflammatory di
136 ally transmitted diseases, and in particular chlamydial infection, can be successfully implemented us
137 gh caspase-1 is not required for controlling chlamydial infection, caspase-1-mediated responses can e
138 s detected in women with lower genital tract chlamydial infection, compared with those with upper gen
139 the mechanisms by which chronic asymptomatic chlamydial infection contribute to atherogenesis.
140 e resistance of CD28 or CD80/CD86 KO mice to chlamydial infection correlated with production of gamma
141 her compared host inflammatory responses and chlamydial infection courses between the hydrosalpinx-re
142                          This indicates that chlamydial infection, despite its intravacuolar location
143 noses derived using participants' reports of chlamydial infections diagnosed during the 12 months pri
144   To study the responses of the host cell to chlamydial infection, differentially transcribed genes o
145 gesting that reduced macrophage responses to chlamydial infection do not always lead to a reduction i
146  women with an appropriately treated initial chlamydial infection during 1993-1998, 15% developed one
147 2), and prior chlamydial infection predicted chlamydial infection during a 6-56-month follow-up perio
148 ha/beta IFN (IFN-alpha/beta) signaling clear chlamydial infection earlier than control mice and devel
149 ed to have either an untreated gonococcal or chlamydial infection, estimated prevalence is substantia
150 fectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations
151 I interferons (IFNs) induced during in vitro chlamydial infection exert bactericidal and immunomodula
152 TGF-beta signaling pathways cooperate during chlamydial infection for optimal inclusion development a
153 rferon (IFN-gamma) in the early clearance of chlamydial infection from the murine female genital trac
154 eptable for identification of gonococcal and chlamydial infections from urine samples, but are not re
155                                 During human chlamydial infection, glucose limitation may decrease ch
156  respondents aged 18-26 years was tested for chlamydial infection, gonorrhea, and trichomoniasis in w
157                       The effect of P2X7R on chlamydial infection had never been investigated in the
158       Although the concept of persistence in chlamydial infections has been recognized for about 80 y
159 PID and long-term sequelae from an untreated chlamydial infection have not been fully determined.
160         Women with symptomless gonorrhoea or chlamydial infection having an IUD inserted have a highe
161 % confidence interval [CI], 0.74 to 1.62) or chlamydial infection (hazard ratio, 0.71; 95% CI, 0.47 t
162                             For detection of chlamydial infection, HC2-RCS had a sensitivity and a sp
163 omic profiling of the macrophage response to chlamydial infection highlighted the role of the type I
164 ndependent predictors of HIV-1 were baseline chlamydial infection (HR, 5.2), bacterial vaginosis (HR,
165 expression in genital mucosae during genital chlamydial infection in a murine model to determine how
166                         Prevalence of ocular chlamydial infection in all children aged 1 to 5 years f
167 dren in trachoma-endemic communities reduces chlamydial infection in both children and untreated adul
168 T cell-dependent pathogenic mechanism during chlamydial infection in C57BL/6J mice.
169                            The prevalence of chlamydial infection in China is substantial.
170 duration of untreated, uncomplicated genital chlamydial infection in humans and the factors associate
171 al ORF-encoded proteins are expressed during chlamydial infection in humans but also providing the pr
172                       The natural history of chlamydial infection in humans, including the duration o
173 ally, as well as their immunogenicity during chlamydial infection in humans.
174 t only expressed but also immunogenic during chlamydial infection in humans.
175 iPSCs, and confirmed their roles in limiting chlamydial infection in macrophages.
176            An RNA-based test detected ocular chlamydial infection in more children than did a DNA-bas
177 S is required for IFN-beta expression during chlamydial infection in multiple cell types.
178 ow-derived DC line, we show that DCs control chlamydial infection in multiple small inclusions charac
179  Interestingly, C5 activation was induced by chlamydial infection in oviducts of C3(-/-) mice, explai
180 ome was persistent or recurrent gonorrhea or chlamydial infection in patients 3 to 19 weeks after tre
181             However, many studies have found chlamydial infection in the absence of clinical disease.
182 evelopment of pathology and on the course of chlamydial infection in the conjunctiva was determined.
183                                              Chlamydial infection in the lower genital tract can lead
184  of oviduct pathology resulting from genital chlamydial infection in the mouse model.
185               We conclude that adequate live chlamydial infection in the oviduct may be necessary to
186 ntibodies to MOMP can protect mice against a chlamydial infection in the presence or absence of T and
187 nstrated to reduce the overall prevalence of chlamydial infection in the tested population and to red
188      Their potential impact on the burden of chlamydial infection in the United States, in light of s
189  in caspase-1 experienced similar courses of chlamydial infection in their urogenital tracts, suggest
190 ply that MMP are involved in pathogenesis of chlamydial infection in this model by mediating ascensio
191 iol decreases susceptibility to intrauterine chlamydial infection in this rat model.
192         We compared the prevalence of ocular chlamydial infection in untreated individuals 11 years a
193 eater understanding of the seroprevalence of chlamydial infection in US populations.
194 tibility of macrophages from iNOS-/- mice to chlamydial infection in vitro.
195 contributing to the most serious sequelae of chlamydial infection in women: pelvic inflammatory disea
196 tudy suggests that efforts to prevent repeat chlamydial infection in young women remain an urgent pub
197 red with ACCESS immunoassay for detection of chlamydial infections in females.
198                                              Chlamydial infections in humans cause severe health prob
199 nificant difference in the course of genital chlamydial infections in iNOS+/+ and iNOS-/- mice as det
200 uld help to characterize the pathogenesis of chlamydial infections in males and to test therapeutic a
201 ctions in women; 84.0%, 87.7%, and 93.1% for chlamydial infections in men; and 55.6%, 91.3%, and 84.9
202 revalence and distribution of gonococcal and chlamydial infections in the general population are poor
203                                Most repeated chlamydial infections in this high-incidence cohort were
204 ng men who have sex with men and over 20% of chlamydial infections in women would have been missed if
205 spectively, were 83.3%, 92.5%, and 79.9% for chlamydial infections in women; 84.0%, 87.7%, and 93.1%
206 ed controlled trials of 1-time screening for chlamydial infection-in a Seattle-area health maintenanc
207 e comparison of trichomonal, gonococcal, and chlamydial infection incidence in participants by Nugent
208 reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and
209 tection against pathological consequences of chlamydial infection, including the development of hydro
210                    We previously showed that chlamydial infection increases markers of autophagy, an
211                                        Adult chlamydial infections induce Th1-type responses that sub
212                                     Although chlamydial infection induced caspase-1 activation and pr
213                 Flow cytometry revealed that chlamydial infection induced cell surface expression of
214                                 Furthermore, chlamydial infection induced the secretion of interleuki
215 ese results indicate that neonatal pulmonary chlamydial infection induces a robust Th1-type response,
216 nduce a rapid cytokine/chemokine production, chlamydial infection induces delayed inflammatory respon
217 med to have frequent and ongoing exposure to chlamydial infection, interferon-g production by periphe
218 ngineered IL-10-/- (IL-10KO) mice to genital chlamydial infection is a function of the predilection o
219    It is well known that pathology caused by chlamydial infection is associated closely with the host
220            Results demonstrated that genital chlamydial infection is associated with a significant in
221                                              Chlamydial infection is common in teenagers and young ad
222                            The prevalence of chlamydial infection is high among young adults in the U
223  female military recruits, the prevalence of chlamydial infection is high.
224                         A vaccine to prevent chlamydial infection is needed but has proven difficult
225                                              Chlamydial infection is the most common sexually transmi
226       The initial host response in a primary chlamydial infection is the onset of acute inflammation.
227 stigate the distribution and determinants of chlamydial infection load in an endemic community, and t
228  age, race, history of prior urethritis, and chlamydial infection, M. genitalium was associated with
229                                        Thus, chlamydial infection may alter the intracellular levels
230                               A history of a chlamydial infection may prove to be a poor guide for th
231                                    In women, chlamydial infections may cause pelvic inflammatory dise
232 e mechanisms by which a chronic asymptomatic chlamydial infection might contribute to the pathophysio
233  and emerging data suggest that asymptomatic chlamydial infections might be a common cause.
234  with current, laboratory confirmed, genital chlamydial infection (n = 98) and one group of individua
235         Persistent or recurrent gonorrhea or chlamydial infection occurred in 121 of 931 patients (13
236                                              Chlamydial infection of the conjunctival, pulmonary, or
237 ulsed DC produce protective immunity against chlamydial infection of the female genital tract equal t
238 s that functioned in resistance to secondary chlamydial infection of the genital tract.
239  These findings demonstrate that subclinical chlamydial infection of the murine female genital tract
240 ed immunity is crucial for the resolution of chlamydial infection of the murine female genital tract.
241 appears to be critical for the resolution of chlamydial infections of the urogenital epithelium.
242  of vATPase-bearing organelles that regulate chlamydial infection: one supports chlamydial infection,
243 oup had 116 diagnosed gonococcal infections, chlamydial infections, or both for a rate of 43.6 per 10
244 tial data demonstrating treatment failure of chlamydial infections, particularly with azithromycin.
245 , multiple sex partners (> or =2), and prior chlamydial infection predicted chlamydial infection duri
246 timated number of undiagnosed gonococcal and chlamydial infections prevalent in the population of Bal
247 y of the transfected cells to the subsequent chlamydial infection, purified pgp3 protein stimulated m
248 or alpha (TNF-alpha) in host defense against chlamydial infection remains unclear.
249 e horn dilation, developed in mice following chlamydial infection remains unclear.
250 om the National Survey of Family Growth, and chlamydial infections reported to the Centers for Diseas
251 st IFN-beta transcription during an in vitro chlamydial infection requires interferon regulatory tran
252     To study the human cellular responses to chlamydial infection, researchers have frequently used t
253           Over 60% and 80% of gonococcal and chlamydial infections, respectively, among men who have
254  more telephone contacts had a lower risk of chlamydial infection (risk ratio = 0.95; 95% CI, 0.90 to
255 g the alternating acute-silent chronic-acute chlamydial infection scenario that exists in infected pa
256 CPAF plus IL-12 resolved the primary genital chlamydial infection significantly earlier than mock-imm
257 showed histological findings consistent with chlamydial infection, such as germinal centers.
258 ine epithelial cells are more susceptible to chlamydial infection than are progesterone-dominant cell
259  be an indicator of severe persistent ocular chlamydial infection that is not cleared with a single d
260                     In all animal models for chlamydial infection, there is strong evidence for immun
261 t protective immunity against murine genital chlamydial infection, thus making CPAF a viable vaccine
262 atified pair-formation transmission model of chlamydial infection to epidemiologic data in the United
263 women and heterosexual men with gonorrhea or chlamydial infection to have their partners receive expe
264 nses at the cervical mucosa that could limit chlamydial infection to the cervix and/or prevent reinfe
265 must be considered when interpreting data on chlamydial infection trends.
266                We show that human and murine chlamydial infection tropism is linked to unique host an
267 WHO simplified grading system and for ocular chlamydial infection using DNA-based and RNA-based tests
268 trachoma, conjunctival swabs were tested for chlamydial infection using GeneXpert platform, and blood
269 anism of IP-10 and IFN-beta induction during chlamydial infection using mouse macrophages and fibrobl
270 ced IFN-beta expression significantly during chlamydial infection using small interfering RNA and gen
271 ndom group was 1.5 (95% CI, 1.0-2.3) and for chlamydial infection was 1.0 (95% CI, 0.7-1.4).
272                                Prevalence of chlamydial infection was 2.2% (CI, 1.8% to 2.8%) and was
273 The overall prevalence per 100 population of chlamydial infection was 2.6 (95% confidence interval [C
274           The overall prevalence of cervical chlamydial infection was 28.5% (206 of 722), and most of
275                 The prevalence of urogenital chlamydial infection was 3.2% (95% confidence interval,
276                        Overall prevalence of chlamydial infection was 4.19% (95% confidence interval
277                            The prevalence of chlamydial infection was 5.3%.
278                    The overall prevalence of chlamydial infection was 9.2 percent, with a peak of 12.
279                 In several studies, repeated chlamydial infection was associated with PID and other r
280                                              Chlamydial infection was detected in 7.2% of the populat
281                                              Chlamydial infection was detected in the glandular epith
282  local and systemic immune systems following chlamydial infection was determined by analyzing major h
283                            The prevalence of chlamydial infection was highest among black women (13.9
284                                Prevalence of chlamydial infection was highest in the south (5.39%; 95
285 tein) may play in the host's defense against chlamydial infection was investigated.
286                                       Ocular chlamydial infection was not eliminated in children aged
287  IL-12p40, and perforin) were increased when chlamydial infection was present.
288 rface heparan sulfate is required to promote chlamydial infection was tested using a cell line (CHO-1
289   In searching for host factors required for chlamydial infection, we discovered that C. trachomatis
290          Test characteristics for predicting chlamydial infection were computed assuming a chlamydial
291   Heterosexual individuals with gonorrhea or chlamydial infection were eligible for the intervention.
292  women aged 20 to 44 years, risk factors for chlamydial infection were having less education (OR, 2.8
293 ribution patterns, and effects on subsequent chlamydial infection when expressed ectopically, as well
294 rance in the murine and guinea pig models of chlamydial infection, which are useful for studying C. t
295 lts suggest that in many patients with uSpA, chlamydial infection, which is often occult, may be the
296 trophil infiltration in mouse airways during chlamydial infection, which may contribute to the antich
297  regulate chlamydial infection: one supports chlamydial infection, while the other plays a defensive
298 sive scarring and whether simply controlling chlamydial infection will halt progression in people wit
299  failed to enhance the resolution of genital chlamydial infection within recipient IFN-gamma receptor
300 pes (n=1211), was associated with coexisting chlamydial infection, younger age, heterosexual contact,

 
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