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1 TNF-alpha released in situ during secondary chlamydial infection.
2 rophils has important effects in vivo during chlamydial infection.
3 y end point was newly acquired gonococcal or chlamydial infection.
4 d to localize the endogenous proteins during chlamydial infection.
5 ve protective immunity against human genital chlamydial infection.
6 significant role for antibody in immunity to chlamydial infection.
7 essure for maintaining pgp3 secretion during chlamydial infection.
8 y without affecting the host defense against chlamydial infection.
9 ng RNA failed to produce IL-8 in response to chlamydial infection.
10 its recommendations regarding screening for chlamydial infection.
11 not play a significant role in resolution of chlamydial infection.
12 r differential susceptibility against murine chlamydial infection.
13 hose with gonorrheal infection, 46% also had chlamydial infection.
14 y selected villages were assessed for ocular chlamydial infection.
15 ys in induction of IP-10 and IFN-beta during chlamydial infection.
16 ates of persistent or recurrent gonorrhea or chlamydial infection.
17 onse by nonimmune cells in host clearance of chlamydial infection.
18 te the host innate antimicrobial response to chlamydial infection.
19 s) in induction of IFN-beta and IP-10 during chlamydial infection.
20 antly to oviduct pathology following genital chlamydial infection.
21 hnicity, and HIV-1 infection did not predict chlamydial infection.
22 s both produced and immunogenic during human chlamydial infection.
23 blasts and production of ECM proteins during chlamydial infection.
24 ctivities have been reported to occur during chlamydial infection.
25 t-catch urines [FCU]) for diagnosing genital chlamydial infection.
26 teractions that may contribute to persistent chlamydial infection.
27 not protect against urogenital gonococcal or chlamydial infection.
28 (SE, 0.8%) is estimated to have an untreated chlamydial infection.
29 cient in their ability to sustain productive chlamydial infection.
30 Yersinia spp., have an inhibitory effect on chlamydial infection.
31 ehavioural determinants of prevalent genital chlamydial infection.
32 he presence of symptoms were associated with chlamydial infection.
33 ollowed by selection for clones resistant to chlamydial infection.
34 ased Th1 response and a shorter, more benign chlamydial infection.
35 mmunotherapeutic vaccination against genital chlamydial infection.
36 n important cytokine in host defense against chlamydial infection.
37 cally in providing immunity in this model of chlamydial infection.
38 egulation of the susceptibility of mice to a chlamydial infection.
39 e as a novel approach to vaccination against chlamydial infection.
40 infection, transmission, and the sequelae of chlamydial infection.
41 ly mimics the immune response produced after chlamydial infection.
42 cells, and adjacent to glands in response to chlamydial infection.
43 unological control may thus exist in genital chlamydial infection.
44 b B6.1 did not affect development of vaginal chlamydial infection.
45 was no high-risk planning region for repeat chlamydial infection.
46 fine the role of PmpD in the pathogenesis of chlamydial infection.
47 allmark of tubal infertility associated with chlamydial infection.
48 of DNA sensors in IFN-beta expression during chlamydial infection.
49 nses previously described for persistence of chlamydial infection.
50 lammasome-activation pathways during genital chlamydial infection.
51 for ASC in adaptive immunity during genital chlamydial infection.
52 elopment of oviduct pathology during genital chlamydial infection.
53 appear sensitive for the detection of ocular chlamydial infection.
54 may preferentially expose females to ocular chlamydial infection.
55 s administered to wild-type (WT) mice during chlamydial infection.
56 optimal oviduct pathology following genital chlamydial infection.
57 ed a Th1/Th17-dominant immune response after chlamydial infection.
58 t result for trichomonal, gonococcal, and/or chlamydial infection.
59 tics, and its laboratory correlates in human chlamydial infection.
60 n the genital tract during the first week of chlamydial infection.
61 s in innate and adaptive immune responses to chlamydial infection.
62 t for the establishment and maintenance of a chlamydial infection.
63 detection of trichomonal, gonococcal, and/or chlamydial infection.
64 response in the female genital tract during chlamydial infection.
65 ost effective strategy for controlling human chlamydial infections.
66 ine or drug targets for the control of human chlamydial infections.
67 al significance to the pathogenesis of human chlamydial infections.
68 at apoptosis has an immunomodulatory role in chlamydial infections.
69 role in the inflammatory processes caused by chlamydial infections.
70 e an important factor in the pathogenesis of chlamydial infections.
71 fections, but not before they resolved their chlamydial infections.
72 e protective or pathological role of CTLs in chlamydial infections.
73 otential to significantly improve control of chlamydial infections.
74 es against trachoma and sexually transmitted chlamydial infections.
75 optimal protective immunity against genital chlamydial infections.
76 t vs. 11 percent, P=0.01) than in those with chlamydial infection (11 percent vs. 13 percent, P=0.17)
77 compared with those with upper genital tract chlamydial infection (13.8% vs 9.5%; P =04), but the CD4
78 ents had single infections (15 gonorrhea, 10 chlamydial infection, 3 trichomoniasis), and 4 had dual
79 (mostly *0602 and *0603) was associated with chlamydial infection (49% vs. 34%; adjusted relative odd
81 han in the comparison condition had incident chlamydial infections (94 vs 104 participants, respectiv
82 for incident trichomonal, gonococcal, and/or chlamydial infection (adjusted hazard ratio [AHR] for in
86 study of the effectiveness of screening for chlamydial infection among nonpregnant women at increase
88 To estimate the prevalence of urogenital chlamydial infection among young, low-income women in no
89 rams have had remarkable success at reducing chlamydial infection and clinical signs of trachoma.
90 ective effector and memory responses against chlamydial infection and demonstrates that an effective
92 ng was associated with a lower prevalence of chlamydial infection and fewer reported cases of pelvic
93 97% when urine samples were tested, for both chlamydial infection and gonorrhea and in both men and w
94 e new information about the pathogenomics of chlamydial infection and insights for improving murine m
95 innate resistance protein in the control of chlamydial infection and may help explain why the macrop
96 roteasome-like activity factor), its role in chlamydial infection and pathogenesis remains unclear.
98 cipants with a laboratory-confirmed incident chlamydial infection and percentage of participants with
101 es (MMPs) would be enhanced following murine chlamydial infection and that their expression would var
102 been implicated in susceptibility to genital chlamydial infection and the development of tubal pathol
103 ing of pulsed dendritic cells to the site of chlamydial infection and the induction of a local protec
104 processing occurred inside live cells during chlamydial infection and was not due to proteolysis duri
105 protein was detected as early as 12 h after chlamydial infection and was present in the inclusion me
106 ion of deleterious immune responses in human chlamydial infections and has been found to colocalize w
107 assessed, conjunctival swabs were tested for chlamydial infection, and blood spots were collected on
108 tween pathogenic and protective responses to chlamydial infection, and genes controlling NO productio
109 or chlamydia, to retest infected females for chlamydial infection, and to co-treat individuals with g
110 ast infection was negatively associated with chlamydial infection (AOR = 0.28; 95% CI = 0.10 to 0.83)
111 of a major category of altered miRNAs during chlamydial infection are key components of the pathophys
115 ny sex partners of persons with gonorrhea or chlamydial infections are not treated, which leads to fr
119 rogression of Chlamydia infections, and with chlamydial infections at record levels in the US, we the
120 Inhibition of MCP-1 is not beneficial in chlamydial infection because of its pleiotropic effects.
122 ction in the early phase of host response to chlamydial infection but also plays a critical role in t
123 n synthesis or trafficking in the absence of chlamydial infection but reduced the amount of sphingomy
124 udies assessed PID diagnosis after untreated chlamydial infection, but rates varied widely, making it
126 asmic reticulum nor inhibition of subsequent chlamydial infection by ectopically expressed proteins c
127 pecimens testing positive for gonococcal and chlamydial infection by ligase chain reaction, weighted
128 hat basal levels of ROS are generated during chlamydial infection by NADPH oxidase, but ROS levels, r
130 ell physiology and thereby susceptibility to chlamydial infection by reverse-stage, exogenous hormona
131 A positive test result for gonococcal or chlamydial infection by the ligase chain reaction assay;
132 lyzed the frequency and predictors of repeat chlamydial infection by using a population-based chlamyd
133 se of sexually transmitted disease in women, chlamydial infections can lead to pelvic inflammatory di
134 ally transmitted diseases, and in particular chlamydial infection, can be successfully implemented us
135 gh caspase-1 is not required for controlling chlamydial infection, caspase-1-mediated responses can e
136 s detected in women with lower genital tract chlamydial infection, compared with those with upper gen
138 e resistance of CD28 or CD80/CD86 KO mice to chlamydial infection correlated with production of gamma
139 her compared host inflammatory responses and chlamydial infection courses between the hydrosalpinx-re
141 noses derived using participants' reports of chlamydial infections diagnosed during the 12 months pri
143 To study the responses of the host cell to chlamydial infection, differentially transcribed genes o
144 gesting that reduced macrophage responses to chlamydial infection do not always lead to a reduction i
145 women with an appropriately treated initial chlamydial infection during 1993-1998, 15% developed one
146 2), and prior chlamydial infection predicted chlamydial infection during a 6-56-month follow-up perio
147 ha/beta IFN (IFN-alpha/beta) signaling clear chlamydial infection earlier than control mice and devel
148 ed to have either an untreated gonococcal or chlamydial infection, estimated prevalence is substantia
149 fectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations
150 I interferons (IFNs) induced during in vitro chlamydial infection exert bactericidal and immunomodula
151 rferon (IFN-gamma) in the early clearance of chlamydial infection from the murine female genital trac
152 eptable for identification of gonococcal and chlamydial infections from urine samples, but are not re
154 respondents aged 18-26 years was tested for chlamydial infection, gonorrhea, and trichomoniasis in w
157 PID and long-term sequelae from an untreated chlamydial infection have not been fully determined.
159 k factors were independently associated with chlamydial infection: having ever had vaginal sex (odds
160 % confidence interval [CI], 0.74 to 1.62) or chlamydial infection (hazard ratio, 0.71; 95% CI, 0.47 t
162 omic profiling of the macrophage response to chlamydial infection highlighted the role of the type I
163 ne responses alone were capable of resolving chlamydial infection; however, in the absence of specifi
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
167 dren in trachoma-endemic communities reduces chlamydial infection in both children and untreated adul
169 duration of untreated, uncomplicated genital chlamydial infection in humans and the factors associate
170 al ORF-encoded proteins are expressed during chlamydial infection in humans but also providing the pr
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
182 evelopment of pathology and on the course of chlamydial infection in the conjunctiva was determined.
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 in caspase-1 experienced similar courses of chlamydial infection in their urogenital tracts, suggest
189 ply that MMP are involved in pathogenesis of chlamydial infection in this model by mediating ascensio
194 contributing to the most serious sequelae of chlamydial infection in women: pelvic inflammatory disea
195 tudy suggests that efforts to prevent repeat chlamydial infection in young women remain an urgent pub
198 nificant difference in the course of genital chlamydial infections in iNOS+/+ and iNOS-/- mice as det
199 uld help to characterize the pathogenesis of chlamydial infections in males and to test therapeutic a
200 ctions in women; 84.0%, 87.7%, and 93.1% for chlamydial infections in men; and 55.6%, 91.3%, and 84.9
201 revalence and distribution of gonococcal and chlamydial infections in the general population are poor
203 ng men who have sex with men and over 20% of chlamydial infections in women would have been missed if
204 spectively, were 83.3%, 92.5%, and 79.9% for chlamydial infections in women; 84.0%, 87.7%, and 93.1%
205 ed controlled trials of 1-time screening for chlamydial infection-in a Seattle-area health maintenanc
206 e comparison of trichomonal, gonococcal, and chlamydial infection incidence in participants by Nugent
207 reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and
208 tection against pathological consequences of chlamydial infection, including the development of hydro
213 ese results indicate that neonatal pulmonary chlamydial infection induces a robust Th1-type response,
214 nduce a rapid cytokine/chemokine production, chlamydial infection induces delayed inflammatory respon
215 med to have frequent and ongoing exposure to chlamydial infection, interferon-g production by periphe
216 ngineered IL-10-/- (IL-10KO) mice to genital chlamydial infection is a function of the predilection o
217 It is well known that pathology caused by chlamydial infection is associated closely with the host
225 stigate the distribution and determinants of chlamydial infection load in an endemic community, and t
226 age, race, history of prior urethritis, and chlamydial infection, M. genitalium was associated with
229 tions provides potential mechanisms by which chlamydial infections may promote atherogenesis and prec
230 e mechanisms by which a chronic asymptomatic chlamydial infection might contribute to the pathophysio
232 with current, laboratory confirmed, genital chlamydial infection (n = 98) and one group of individua
236 ulsed DC produce protective immunity against chlamydial infection of the female genital tract equal t
240 These findings demonstrate that subclinical chlamydial infection of the murine female genital tract
241 ed immunity is crucial for the resolution of chlamydial infection of the murine female genital tract.
242 appears to be critical for the resolution of chlamydial infections of the urogenital epithelium.
243 of vATPase-bearing organelles that regulate chlamydial infection: one supports chlamydial infection,
244 negative STD clinic patients with gonorrhea, chlamydial infection, or trichomoniasis were compared wi
245 oup had 116 diagnosed gonococcal infections, chlamydial infections, or both for a rate of 43.6 per 10
247 tial data demonstrating treatment failure of chlamydial infections, particularly with azithromycin.
248 , multiple sex partners (> or =2), and prior chlamydial infection predicted chlamydial infection duri
249 timated number of undiagnosed gonococcal and chlamydial infections prevalent in the population of Bal
250 y of the transfected cells to the subsequent chlamydial infection, purified pgp3 protein stimulated m
253 om the National Survey of Family Growth, and chlamydial infections reported to the Centers for Diseas
254 st IFN-beta transcription during an in vitro chlamydial infection requires interferon regulatory tran
256 idence interval [CI] = 1.05-1.43) and repeat chlamydial infection (RH = 1.78; 95% CI = 1.23-2.57).
257 more telephone contacts had a lower risk of chlamydial infection (risk ratio = 0.95; 95% CI, 0.90 to
258 g the alternating acute-silent chronic-acute chlamydial infection scenario that exists in infected pa
259 CPAF plus IL-12 resolved the primary genital chlamydial infection significantly earlier than mock-imm
261 ine epithelial cells are more susceptible to chlamydial infection than are progesterone-dominant cell
262 be an indicator of severe persistent ocular chlamydial infection that is not cleared with a single d
264 t protective immunity against murine genital chlamydial infection, thus making CPAF a viable vaccine
265 women and heterosexual men with gonorrhea or chlamydial infection to have their partners receive expe
268 WHO simplified grading system and for ocular chlamydial infection using DNA-based and RNA-based tests
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
273 The overall prevalence per 100 population of chlamydial infection was 2.6 (95% confidence interval [C
282 local and systemic immune systems following chlamydial infection was determined by analyzing major h
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
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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