ライフサイエンスコーパス: genital tract

1 y correlated with pathogenicity in the upper genital tract.

2 rum compared to C. trachomatis in the murine genital tract.

3 to serve as a live attenuated vaccine in the genital tract.

4 ction versus driving inflammation within the genital tract.

5 (+) T cells and dendritic cells in the lower genital tract.

6 ar mechanisms of action of MPA in the female genital tract.

7 blood and CSF and between blood and the male genital tract.

8 anded and/or recruited T cells in the female genital tract.

9 out inducing immune pathologies in the upper genital tract.

10 leads to recurrent shedding episodes in the genital tract.

11 ell response to C. trachomatis in the murine genital tract.

12 es in efficiency of ascension into the upper genital tract.

13 butes to chronic inflammation throughout the genital tract.

14 an support Lactobacillus colonization in the genital tract.

15 luble defense responses to GBS in the female genital tract.

16 d be utilized by vaginal lactobacilli in the genital tract.

17 butes to chronic inflammation throughout the genital tract.

18 l tract and shortened infection in the upper genital tract.

19 the immunopathogenesis of HIV in the female genital tract.

20 muridarum cannot directly autoinoculate the genital tract.

21 t HIV is compartmentalized within the female genital tract.

22 2) is periodically shed throughout the human genital tract.

23 by lowering the concentration of HIV in the genital tract.

24 including barrier sites such as the skin and genital tract.

25 ined robust ascending infection of the upper genital tract.

26 such viruses were also detected in the donor genital tract.

27 immunity against Chlamydia infections of the genital tract.

28 contribute to its pathogenicity in the upper genital tract.

29 of neutrophils, but more macrophages, in the genital tract.

30 rpesviruses known to be shed from the female genital tract.

31 molecules were still detectable in the upper genital tract.

32 also seems to affect those that home to the genital tract.

33 developed more severe pathology in the upper genital tract.

34 ntly at widely spaced regions throughout the genital tract.

35 ydia muridarum in both mouse lung and female genital tract.

36 with diverse roles in function of the female genital tract.

37 itical for clearing bacteria from the murine genital tract.

38 ole in mucosal HIV-1 infection in the female genital tract.

39 is the most common malignancy of the female genital tract.

40 ly due to unique viruses evolving within the genital tract.

41 systemically and, for the first time, in the genital tract.

42 cific mRNA within Drosophila testes and male genital tract.

43 et of internal sensory neurons in the female genital tract.

44 th its attenuated pathogenicity in the upper genital tract.

45 nal tract and its pathogenicity in the upper genital tract.

46 s of proinflammatory immune mediators in the genital tract.

47 were directly delivered into the mouse upper genital tract.

48 L-1beta, and IL-17A production in the female genital tract.

49 isk and the immune environment in the female genital tract.

50 ing host-pathogen interactions in the female genital tract.

51 ses at barrier tissues, including the female genital tract.

52 to their abilities to ascend the guinea pig genital tract.

53 nfluence pathology and immunity in the upper genital tract.

54 variations in immune responses in the female genital tract.

55 e bacterial loads of the two variants in the genital tract.

56 help counter HIV-1 acquisition in the female genital tract.

57 vention of pathological changes in the upper genital tract.

58 are dispensable for infection of the murine genital tract.

59 evaluate HIV-1 acquisition across the female genital tract.

60 chlamydial organisms from the lower to upper genital tracts.

61 survival of the plasmidless organisms in the genital tracts.

62 g C. trachomatis survival in the mouse lower genital tracts.

63 Epithelial cells lining the murine genital tract act as sentinels for microbial infection,

64 administered dose was retained in the female genital tract after 4 hours.

65 ns and lower levels of viral shedding in the genital tract after HSV-2 challenge.

66 understanding HIV distribution in the female genital tract after intercourse.

67 C) remains the most common malignancy of the genital tract among women in developed countries.

68 rom widely separated anatomic regions of the genital tract and are associated with a localized cellul

69 s women, HIV lineages were comprised of both genital tract and blood sequences.

70 Compartmentalization of virus between genital tract and blood was observed by statistical meth

71 terchange of HIV variants between the female genital tract and blood.

72 ages do not form; rather viruses mix between genital tract and blood.

73 ve dosing strategies to protect lower female genital tract and colorectal tissues.

74 copulation, frequently bypassing the female genital tract and ejaculating into their blood system.

75 alpha-amylase is present in the female lower genital tract and elucidates how epithelial glycogen can

76 chronic inflammatory diseases of the eye and genital tract and has global medical importance.

77 levels of interleukin 8 (IL-8) in the lower genital tract and increased leukocyte infiltration in th

78 ph nodes, small bowel, nasal turbinates, the genital tract and lung.

79 enospecies is an important cause of maternal genital tract and neonatal systemic infections and initi

80 homatis is also attenuated in both the mouse genital tract and nonhuman primate ocular tissue.

81 Chorioamnionitis frequently precedes both genital tract and placental inflammation and is both a p

82 averses the protective barriers of the human genital tract and presents a second mechanism whereby gp

83 decrease in chlamydial survival in the lower genital tract and reduced ascension to the upper genital

84 uired for C. muridarum survival in the mouse genital tract and represents a major virulence factor in

85 educed live organism recovery from the lower genital tract and shortened infection in the upper genit

86 persistence of N. gonorrhoeae in the female genital tract and that opa gene phase variation allows g

87 ut where and how IgG enters the lumen of the genital tract and the exact role local IgG plays in prev

88 myoma is the most common tumor of the female genital tract and the leading cause of hysterectomy.

89 common colonizer of the gastrointestinal and genital tracts and an important cause of invasive infect

90 nly colonizes the lower gastrointestinal and genital tracts and, during pregnancy, neonates are at ri

91 counts, having bacterial coinfections in the genital tract, and not using antiretroviral therapy.

92 nal discharge, detectable HIV-1 RNA in their genital tracts, and lower blood CD4 counts.

93 It is not known if fluctuations in genital tract antiretroviral drug concentrations correla

94 ex virus type 2 (HSV-2) reactivations in the genital tract are responsible for mucocutaneous lesions

95 l tract; however, AZ2 was able to ascend the genital tract as readily as SP6.

96 ased into semen by various cells of the male genital tract, as well as by infected monocytes and lymp

97 ne samples contained mixtures of urinary and genital tract bacteria.

98 nisms were directly delivered into the upper genital tract, both confirming the role of C5 in promoti

99 rum retains the ability to infect the murine genital tract but does not elicit oviduct pathology beca

100 nfection and reducing pathology of the upper genital tract by chlamydial organisms.

101 ation of XXI prevents infection of the mouse genital tract by human papillomavirus type 16 (HPV16) ps

102 Chlamydia trachomatis infection in the lower genital tract can ascend to and cause pathologies in the

103 Chlamydial infection in the lower genital tract can lead to hydrosalpinx, which is accompa

104 hlamydia infections that ascend to the upper genital tract can persist, trigger inflammation, and res

105 We utilized a murine genital tract carriage model to demonstrate that M1 and

106 Genital tract carriage of group B streptococcus (GBS) is

107 women; however, the dynamics of chronic GBS genital tract carriage, including how GBS persists in th

108 that chronic GBS colonization of the murine genital tract caused significant lymphocyte and PMN cell

109 burdens that naturally ascended to the upper genital tract, causing salpingitis.

110 helial and neuronal cells, including primary genital tract cells and human fetal neurons and astrocyt

111 tochemistry studies that showed extant upper genital tract Chlamydia infection was associated with in

112 Also among women with genital tract Chlamydia infection, peripheral CD3(+) CD4

113 al infection, compared with those with upper genital tract chlamydial infection (13.8% vs 9.5%; P =04

114 l responses was detected in women with lower genital tract chlamydial infection, compared with those

115 Thus, we have demonstrated that the genital tract chlamydial organisms may use a systemic ro

116 Redundant genital tract clearance mechanisms bring into question n

117 hormonal contraceptive use, sexual behavior, genital tract coinfection, and Papanicolaou test results

118 amics in a novel murine model of chronic GBS genital tract colonization and establishes previously un

119 report the first animal model of chronic GBS genital tract colonization using female mice synchronize

120 showed that the host response to GBS in the genital tract comprised markers of innate immune activat

121 t effectors in the innate defence of the uro-genital tract creates new translational possibilities fo

122 Here, we demonstrate that genital tract-derived cell lines and primary human endoc

123 ld provide mucosal surface protection in the genital tract, develop assays for vaccine potency, and u

124 and localization of HIV/SIV within the male genital tract, discuss the potential involvement of each

125 mportant question in the study of chlamydial genital tract disease is why some women develop severe u

126 women infected with chlamydiae develop upper genital tract disease, but the reason(s) for this remain

127 athogen responsible for both male and female genital tract disease.

128 as psychiatric, inflammatory, metabolic, and genital tract diseases, need to be addressed.

129 mouse do not ascend efficiently to the upper genital tract, do not cause persistent infection, do not

130 pecific CD8(+) T cells, detected in both the genital tract draining nodes and in the vaginal mucosa;

131 r of the inflammatory response in the female genital tract during chlamydial infection.

132 cant levels of inflammatory cytokines in the genital tract during the first week of chlamydial infect

133 host antimicrobial peptide secreted by both genital tract epithelial cells and infiltrating neutroph

134 al Fc receptor, FcRn, is expressed in female genital tract epithelial cells of humans and mice and bi

135 SV-1 and HSV-2 in human cervical and primary genital tract epithelial cells.

136 ing pathways the virus usurps to enter human genital tract epithelial cells.

137 Exposure of human cervical and primary genital tract epithelial, neuronal, or keratinocyte cell

138 ogenital serovars replicate predominantly in genital tract epithelium.

139 elicit an inflammatory response in the lower genital tract facilitates the spread of both variants to

140 The female genital tract (FGT) microbiome may affect vaginal pH and

141 The female genital tract (FGT) provides a means of entry to pathoge

142 tionality of multiple transporters in female genital tract (FGT), colorectal tissue, and immune cells

143 m and the composition of the male and female genital tract fluids.

144 sh a successful infection in the mouse lower genital tract following an intravaginal inoculation.

145 Viable M. genitalium persisted in the lower genital tract for 8 weeks in three animals, 4 weeks in t

146 We sampled the genital tract for HSV DNA at several time intervals and

147 chomatis strain (L2-5) survived in the lower genital tract for more than 3 weeks.

148 CD8(+) T cell immunity to protect the female genital tract from herpes.

149 e host defense mechanisms protect the female genital tract from pathogens, but the impact of sexual i

150 obe whether limited genetic diversity in the genital tract (GT) of the transmitting partner drives th

151 receptors expressed by CD4(+) T cells in the genital tract have been characterized, the integrin rece

152 lture and are cleared faster from the murine genital tract, highlighting the importance of CpoS for C

153 Lower genital tract HIV-1 infection after HIV-Du151.2env-NLuc

154 infection, SP6 outcompeted AZ2 in the lower genital tract; however, AZ2 was able to ascend the genit

155 nation antiretroviral therapy (cART) reduces genital tract human immunodeficiency virus type 1 (HIV-1

156 The cervix is central to the female genital tract immune response to pathogens and foreign m

157 V) may experience an immediate disruption of genital tract immunity, altering the ability to mount a

158 hat HIV infection has an immediate impact on genital tract immunity, as evidenced by the high risk of

159 cine platform induces gene expression in the genital tract in both cynomolgus and rhesus macaques.

160 Infections of the lower genital tract in heterozygous (immunocompetent) mice of

161 m by which IgG can act locally in the female genital tract in immune surveillance and in host defense

162 tal tract and reduced ascension to the upper genital tract in mice infected with C. muridarum deficie

163 was observed that NK cells recruited to the genital tract in MyD88 KO mice failed to produce gamma i

164 s (CMV) replication occurs frequently in the genital tract in untreated HIV-infected men and is assoc

165 uridarum induces hydrosalpinx in mouse upper genital tract, indicating a critical role of the plasmid

166 igh concentrations of HCO3 (-) in the female genital tract induce an increase in sperm beat frequency

167 Genital tract infection (31.0%) and the organism Escheri

168 s between race and endometritis and/or upper genital tract infection (UGTI) were explored.

169 However, the mechanisms of GAS genital tract infection are not well understood.

170 eJ mice results in a typical course of lower genital tract infection but, unlike a pathogenic isogeni

171 This implies that resolution of genital tract infection depends on CD4 T-cell interactio

172 mechanism to effectively control chlamydial genital tract infection despite a reduced Th1 response.

173 uide investigation, an experimental model of genital tract infection has been developed in female mic

174 infection, but its role during C. muridarum genital tract infection has not been described.

175 y competed with CM972 during lower and upper genital tract infection in the mouse, demonstrating that

176 Chlamydia trachomatis genital tract infection is a major cause of female repro

177 Resolution of Chlamydia genital tract infection is delayed in the absence of MyD

178 of pre-existing Tregs prior to C. muridarum genital tract infection markedly reduced the frequency a

179 re or were profoundly attenuated in a murine genital tract infection model.

180 he human urethral-challenge and murine lower genital tract infection models.

181 tissue from women with or without Chlamydia genital tract infection to better define this response.

182 Lower genital tract infection with Chlamydia trachomatis and C

183 em and a murine model of Chlamydia muridarum genital tract infection.

184 MyD88 was necessary for normal resolution of genital tract infection.

185 of a well-established small-animal model of genital tract infection.

186 nce for antibody-mediated protection against genital tract infection.

187 es that cause trachoma, sexually transmitted genital tract infections (chlamydia), and invasive lymph

188 Genital tract infections and fluctuations in cervical an

189 Lower genital tract infections caused by both sexually and not

190 Genital tract infections caused by Neisseria gonorrhoeae

191 iterature pertaining to clearance of primary genital tract infections in animal models, including mic

192 Haemophilus cryptic genospecies (HCG) causes genital tract infections in pregnant and postpartum wome

193 ficient to clear primary Chlamydia muridarum genital tract infections in the mouse model, making a pr

194 and treatment of HIV-related conditions and genital tract infections may decrease the risk of HIV-1

195 yl-l-arginine were largely unable to resolve genital tract infections over 8 wk.

196 birth, yet the attributable risk for female genital tract infections remains to be defined.

197 elopmental disorders, asthma, pneumonia, and genital tract infections were among the most common como

198 Urinary and genital tract infections were more common with SGLT2 inh

199 ce mechanisms singly sufficient for clearing genital tract infections within six weeks; one dependent

200 productively infected with Chlamydia during genital tract infections, the overall goal of our resear

201 in resolving C. trachomatis and C. muridarum genital tract infections, we used the female mouse model

202 mised in their ability to clear C. muridarum genital tract infections.

203 or clearing experimental Chlamydia muridarum genital tract infections.

204 n that CD4 T cells are critical for clearing genital tract infections.

205 cted with these strains developed productive genital tract infections.

206 ing cells (APC) of mice that cleared primary genital tract infections.

207 adjusting for sexual behavior and concurrent genital tract infections.

208 and sufficient to clear Chlamydia muridarum genital tract infections.

209 T cell mechanisms for clearing C. muridarum genital tract infections: one dependent on iNOS, and the

210 ibility to SHIV, likely because of prolonged genital tract inflammation.

211 There was an increase in genital tract inflammatory cells, cytokines, chemokines,

212 ermatozoa are exposed in the male and female genital tract influence CatSper activation via modulatio

213 Multiple viruses coinfect the male genital tract, influencing each other's replication and

214 rns of anatomic reactivation, we divided the genital tract into a 22-region grid and obtained daily s

215 ring when the bacteria ascend from the lower genital tract into the uterus and fallopian tubes.

216 The female genital tract is a portal of entry for sexual HIV transm

217 Elevated inflammation in the female genital tract is associated with increased HIV risk.

218 ficiency type 1 (HIV) genotypes occur in the genital tract is important for vaccine development and m

219 , proinflammatory cytokine production in the genital tract is necessary for target cell recruitment a

220 Colonization by Lactobacillus in the female genital tract is thought to be critical for maintaining

221 uman papillomaviruses (HPVs) associated with genital tract lesions have been extensively studied, stu

222 ymptomatic HSV-2 infection shed virus in the genital tract less frequently than persons with symptoma

223 asymptomatic CMV replication within the male genital tract, levels of inflammation in blood, and the

224 at induce memory T and B cells in the female genital tract may prevent the establishment and systemic

225 local immune activation in the lower female genital tract may promote viral replication and genital

226 The female genital tract may serve as a reservoir of persistent HIV

227 anges to the mucosal epithelia of the female genital tract mediate the course of gonococcal disease.

228 cell-mediated immune (CMI) responses in the genital tract mucosa.

229 -33, -35, -52, -58, or -67) detected in the genital tract (n = 156).

230 ability of the strains to proliferate in the genital tract of cows.

231 elected in a cyclical pattern from the lower genital tract of estradiol-treated mice.

232 attenuated disease development in the upper genital tract of female mice.

233 teins from virus isolated from the blood and genital tract of five men with compartmentalized lineage

234 and higher concentration of HIV-1 RNA in the genital tract of HIV-1-infected women.

235 V and cytomegalovirus [CMV] in the blood and genital tract of HIV-infected ART-suppressed subjects.

236 covaginal tissue explants, and in the female genital tract of humanized mice.

237 The Env proteins isolated from the genital tract of subject C018 were macrophage-tropic pro

238 nduce long-lasting hydrosalpinx in the upper genital tract of women and female mice, respectively.

239 However, when applied to the genital tracts of living female macaques, SEVI did not e

240 pathogenesis is clearly demonstrated in the genital tracts of mice infected with Chlamydia muridarum

241 can be isolated from the gastrointestinal or genital tracts of up to 30% of healthy adults, and infec

242 am-positive bacteria that colonize the lower genital tracts of women and are frequently associated wi

243 By contrast, some isolates from the healthy genital tract often lack many of these virulence factors

244 t was compared to those of isolates from the genital tract or brain of dogs.

245 tial role for gastrointestinal chlamydiae in genital tract pathogenicity.

246 n and no longer are able to induce the upper genital tract pathologies, indicating a significant role

247 trachomatis in some women can lead to upper genital tract pathologies, such as hydrosalpinx, potenti

248 or developed for blocking LL-37-involved non-genital-tract pathologies, such as rosacea and psoriasis

249 tion and low incidence and severity of upper genital tract pathology following intravaginal inoculati

250 either susceptibility or resistance to upper genital tract pathology, which will help us to further u

251 ascend to and cause pathologies in the upper genital tract, potentially leading to severe complicatio

252 ctobacillus colonization of the lower female genital tract provides protection from the acquisition o

253 cal chemokine application to the restrictive genital tract (pull), where such T cells establish a lon

254 2 specific T cells persist at prior sites of genital tract reactivation and, in conjunction with prom

255 man immune cell reconstitution of the female genital tract renders these mice susceptible to intravag

256 ia muridarum in mice can ascend to the upper genital tract, resulting in hydrosalpinx, a pathological

257 e that C. trachomatis infection of the upper genital tract results in recruitment of Chlamydia-specif

258 c IgA, but not IgG, has been detected in the genital tract, seminal fluid, urethral swabs, urine, and

259 es, carrying the potential for postinfection genital tract sequelae.

260 value decomposition (SVD) to interpret HSV-2 genital tract shedding time series data, as well as simu

261 athogenicity with ascending infection in the genital tract, since attenuated C. muridarum spread sign

262 Tissues such as the genital tract, skin, and lung act as barriers against in

263 Recovery of viable M. genitalium from lower genital tract specimens was improved by diluting the spe

264 C. trachomatis infection of the murine upper genital tract stimulates a robust Chlamydia-specific CD4

265 hage-tropic lineage of HIV-1 within the male genital tract strongly suggests that evolution of macrop

266 detected at multiple bilateral sites in the genital tract, suggesting that HSV establishes latency t

267 t with chlamydial pathogenicity in the upper genital tract suggests a potential role for gastrointest

268 igher gp140-specific IgA titre in the female genital tract than unconjugated antigen.

269 an inflammation-like response in the female genital tract that activates immune adaptations to advan

270 d address the compensatory mechanisms in the genital tract that ultimately clear infection in the abs

271 chlamydial inclusions were observed in lower genital tract tissue by immunohistochemical staining.

272 ch contributes to the development of chronic genital tract tissue damage.

273 k (85%) was required to protect lower female genital tract tissue from HIV, while adherence to 2 of 7

274 ant facilitator of HIV-1 transcytosis across genital tract tissue.

275 ecruitment of an effector cell population to genital tract tissue.

276 activation of an effector cell population in genital tract tissues by CD4(+) T cells.

277 amydial organisms were detected in the upper genital tract tissues of MyD88 KO mice.

278 ells in vivo independently of proximal upper genital tract tissues.

279 sponse to C. trachomatis in the human female genital tract to control infection and minimize immunopa

280 CD4(+) T cells must home successfully to the genital tract to exert their effector function and decre

281 r Chlamydia muridarum dissemination from the genital tract to the gastrointestinal (GI) tract.

282 wn that Chlamydia muridarum spreads from the genital tract to the gastrointestinal tract potentially

283 pathogenesis, readily spreads from the mouse genital tract to the gastrointestinal tract, establishin

284 symptomatic and do not cause permanent upper genital tract (UGT) damage.

285 chlamydial clearance and reduction of upper genital tract (UGT) pathological sequelae.

286 In men, pathogens can also spread to the genital tract via the continuous ductal system, elicitin

287 wn about the efficacy of cART for decreasing genital tract viral load (GTVL) and differences in sex o

288 Neutrophil influx into the genital tract was also decreased.

289 F-dependent chlamydial survival in the lower genital tract was confirmed in multiple strains of mice.

290 itionally, recruitment of CD4 T cells to the genital tract was reduced in MyD88 KO mice compared to t

291 d the chemokine-cytokine network in the male genital tract, we measured the concentrations of 21 cyto

292 o accumulate in the draining lymph nodes and genital tract when exposed to the same inflammatory mili

293 ss in mucosal secretions of the human female genital tract, where it predominates over the IgA isotyp

294 0 times higher than that in the lower female genital tract, whereas concentrations of endogenous nucl

295 The female genital tract, which is a portal of entry for sexually t

296 tion of C. muridarum directly into the upper genital tract, which resulted in a delayed vaginal shedd

297 within the body, including within the female genital tract with its central role in heterosexual and

298 argeting of the mucosal immune system of the genital tract with subunit vaccines has failed to induce

299 responses were induced in the lungs and the genital tract with the optimized GC-coated LPN adjuvant

300 organisms were cleared from the mouse lower genital tract within a few days, while a CPAF-sufficient