ライフサイエンスコーパス: genital tract

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

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

3 th its attenuated pathogenicity in the upper genital tract.

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

5 s of proinflammatory immune mediators in the genital tract.

6 were directly delivered into the mouse upper genital tract.

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

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

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

10 on in the gastrointestinal tract than in the genital tract.

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

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

13 variations in immune responses in the female genital tract.

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

15 and maintain its pathogenicity in the upper genital tract.

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

17 vention of pathological changes in the upper genital tract.

18 are dispensable for infection of the murine genital tract.

19 itis on the HIV-1 population within the male genital tract.

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

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

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

23 ction versus driving inflammation within the genital tract.

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

25 the microbiological environment in the lower genital tract.

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

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

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

29 out inducing immune pathologies in the upper genital tract.

30 leads to recurrent shedding episodes in the genital tract.

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

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

33 butes to chronic inflammation throughout the genital tract.

34 an support Lactobacillus colonization in the genital tract.

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

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

37 butes to chronic inflammation throughout the genital tract.

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

39 the immunopathogenesis of HIV in the female genital tract.

40 t HIV is compartmentalized within the female genital tract.

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

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

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

44 HIV replication as the cause of DS from the genital tract.

45 rucial for GAS fitness in the female primate genital tract.

46 immunity against Chlamydia infections of the genital tract.

47 vation for antigonococcal Ab function in the genital tract.

48 rachomatis when it is deposited in the lower genital tract.

49 scriptional responses in cells that line the genital tract.

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

51 nfluence pathology and immunity in the upper genital tract.

52 y correlated with pathogenicity in the upper genital tract.

53 muridarum cannot directly autoinoculate the genital tract.

54 ined robust ascending infection of the upper genital tract.

55 contribute to its pathogenicity in the upper genital tract.

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

57 chlamydial organisms from the lower to upper genital tracts.

58 survival of the plasmidless organisms in the genital tracts.

59 We studied HIV-1 reactivation in the female genital tract, a dynamic anatomical target for HIV-1 inf

60 te or chronic inflammation of the urinary or genital tract, abdominal pain, abdominal mass, obstructi

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

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

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

64 while the chlamydial mutant infection in the genital tract alone was unable to induce any significant

65 e attenuated in inducing hydrosalpinx in the genital tract also reduce their colonization in the gast

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

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

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

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

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

71 te of infection, GAS can colonize the female genital tract and cause severe diseases, such as puerper

72 impaired in ability to colonize the primate genital tract and cause uterine wall pathologic findings

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 obiomial composition higher up in the female genital tract and in the fallopian tubes (the site of or

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

79 ated, but not naive, CD8(+) T cells into the genital tract and induced in situ proliferation and diff

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

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

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

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

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

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

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

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

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

89 show that viral populations within the male genital tract are defined by factors beyond transient in

90 Our study highlights the male genital tract as a local source of HIV that can be rever

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

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

93 lts in higher bacterial burdens in the upper genital tract at earlier time points, correlating with l

94 nable chlamydial evasion of the female lower genital tract barrier during sexual transmission.

95 to study the HIV-1 population in the female genital tract before virus is detectable in the bloodstr

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

97 8, paralleling their infection course in the genital tract, but persisted in the large intestine for

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

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

100 hlamydia trachomatis infection of the female genital tract can lead to irreversible fallopian tube sc

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

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

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

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

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

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

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

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

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

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

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

112 Redundant genital tract clearance mechanisms bring into question n

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

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

115 Higher HIV RNA molecular diversity in the genital tract (compared to that in blood plasma) and evi

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

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

118 Time to NAAT clearance of rectal and genital tract CT was similar, and intermittent rectal CT

119 In the genital tract, deficiency in pGP3 significantly reduced

120 herpes simplex virus-2 (HSV-2) in the human genital tract despite low CD8+ and CD4+ tissue-resident

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

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

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

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

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

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

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

128 ttle HIV-1 diversity in the blood and female genital tract during the first 2 weeks after virus was d

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

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

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

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

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

134 centrations of antiretrovirals in the female genital tract (FGT) are critical for suppression of vira

135 Female genital tract (FGT) inflammation increases HIV infection

136 Dysbiosis in the female genital tract (FGT) is characterized by the overgrowth o

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

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

139 ized HIV-1 diversity in the blood and female genital tract (FGT) within 2 weeks after detection of in

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

141 te a role for TLR3 signaling in limiting the genital tract fibrosis, scarring, and chronic inflammati

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

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

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

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

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

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

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

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

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

151 Hormonal contraceptives may increase genital tract HIV viral load (gVL) and sexual transmissi

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

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

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

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

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

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

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

159 ressed predominantly by luminal cells of the genital tract in response to infection, and low levels o

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

161 l, chlamydial organisms are cleared from the genital tract in ~4 weeks, but the genital organisms can

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

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

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

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

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

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

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

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

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

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

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

173 nstrated significant attenuation in a murine genital tract infection model.

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

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

176 Lower genital tract infection with Chlamydia trachomatis and C

177 6J mice are susceptible to a transient lower genital tract infection with MmuPV1 mouse papillomavirus

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

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

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

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

182 Lower genital tract infections caused by both sexually and not

183 The T-cell response to chlamydia genital tract infections in humans and mice is unusual b

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

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

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

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

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

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

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

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

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

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

194 r immunopathology during Chlamydia muridarum genital tract infections.

195 or clearing experimental Chlamydia muridarum genital tract infections.

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

197 cted with these strains developed productive genital tract infections.

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

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

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

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

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

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

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

205 We conclude that the male genital tract is a site where virus can be brought in fr

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

207 can productively infect mice when the lower genital tract is bypassed and bacteria are deposited dir

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

209 ibute to interaction with the primate female genital tract is limited by the lack of relevant animal

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

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

212 hich can cause fibrotic pathology in women's genital tracts, is also frequently detected in the gastr

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

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

215 l Chlamydia failed to directly spread to the genital tract lumen, suggesting that gastrointestinal Ch

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

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

218 y of tenofovir alafenamide (TAF) in the male genital tract (MGT) and the semen quality of individuals

219 se may influence HIV risk through changes in genital tract microbiota and inflammatory cytokines.

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

221 olonization site from the oral cavity to the genital tract of a human or humanoid and had to evolve m

222 -positive bacterium that colonizes the lower genital tract of approximately 18% of women globally as

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

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

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

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

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

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

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

230 ive morbidities after ascending to the upper genital tract of women, and repeated infection can lead

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

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

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

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

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

236 The genital tract pathogen Chlamydia trachomatis is frequent

237 Although Chlamydia trachomatis is a human genital tract pathogen, chlamydial organisms have freque

238 hlamydial replication and possibly increased genital tract pathogenesis during human infection.

239 mechanisms associated with Chlamydia-induced genital tract pathogenesis in humans, we used CRISPR gen

240 tial role for gastrointestinal chlamydiae in genital tract pathogenicity.

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

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

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

244 This correlated with the increased genital tract pathology observed in mice infected at ZT3

245 mydia might induce the second hit to promote genital tract pathology, and we are now providing experi

246 us cause of tubal infertility, induces upper genital tract pathology, such as hydrosalpinx, which can

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

248 Both mutants are attenuated in inducing genital tract pathology.

249 inal Chlamydia in promoting pathology in the genital tract possibly via an indirect mechanism.

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

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

252 2 specific T cells persist at prior sites of genital tract reactivation and, in conjunction with prom

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

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

255 y lead to fibrotic blockage in women's upper genital tracts, resulting in tubal infertility.

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

257 Single viral templates from blood plasma and genital tract RNA and DNA were sequenced across HIV-1 en

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 partners, indicating a lack of evidence for genital tract-specific lineages.

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

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

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

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

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

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

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

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

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

277 ine Chlamydia readily spreads from the mouse genital tract to the gastrointestinal tract while induci

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

279 hanisms by which GBS traffics from the lower genital tract to vulnerable host niches are not well und

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

281 re genetically similar to both the blood and genital tract variants of their male partners, indicatin

282 und in blood are likely to also protect from genital tract variants.

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

284 cteria are deposited directly into the upper genital tract via transcervical inoculation.

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

286 The plasmid-encoded pGP3, a genital tract virulence factor, is essential for Chlamyd

287 ose that chlamydial chromosomal-gene-encoded genital tract virulence factors may be essential for Chl

288 erting female partners found that the males' genital tract viruses were rarely distinct from the bloo

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

290 rrelated with its pathogenicity in the upper genital tract, we evaluated the effect of FTY720 on chla

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

294 ed increased chlamydial burdens in the upper genital tract, which correlated with increased CD4 T cel

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

296 We studied HIV-1 reactivation in the female genital tract, which is often the portal of HIV-1 entry

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

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