ライフサイエンスコーパス: muridarum

1 ision of Chlamydia trachomatis and Chlamydia muridarum.

2 lowing intravaginal infection with Chlamydia muridarum.

3 induction of long-lasting hydrosalpinx by C. muridarum.

4 t, but not inoculation with plasmid-free, C. muridarum.

5 imals were challenged intravaginally with C. muridarum.

6 th 10(4) inclusion-forming units (IFU) of C. muridarum.

7 itro infection of primed macrophages with C. muridarum.

8 sed by the animal pathogens C. caviae and C. muridarum.

9 h plasmid loss in both C. trachomatis and C. muridarum.

10 e ISA 720; then they were challenged with C. muridarum.

11 cells, and then challenged vaginally with C. muridarum.

12 he obligate intracellular pathogen Chlamydia muridarum.

13 s but is absent from inclusions formed by C. muridarum.

14 the closely related mouse pathogen Chlamydia muridarum.

15 duct disease upon challenge with virulent C. muridarum.

16 were infected intravaginally with Chlamydia muridarum.

17 intrauterine infection with plasmid-free C. muridarum a suitable model for investigating plasmid-ind

18 nital tracts of mice infected with Chlamydia muridarum, a model for investigating the human pathogen

19 Chlamydia muridarum, a model pathogen for investigating C. trachom

20 8 gene of serial in vitro-passaged Chlamydia muridarum, a murine model of human urogenital C. trachom

21 e genomic and phenotypic perturbations to C. muridarum, a starter population was passaged in cultured

22 vars of C. trachomatis, as well as Chlamydia muridarum and Chlamydia caviae.

23 The native plasmid of both Chlamydia muridarum and Chlamydia trachomatis has been shown to co

24 Chlamydia muridarum and Chlamydia trachomatis mouse models of geni

25 hysterectomized mice infected with Chlamydia muridarum and Chlamydia trachomatis to determine if ther

26 lls that respond to a common Ag in Chlamydia muridarum and Chlamydia trachomatis Using an adoptive-tr

27 e 18-week study, while mice infected with H. muridarum and H. bilis were negative by ELISA.

28 pylori-infected mice, mice infected with H. muridarum and H. pylori (HmHp mice) developed significan

29 s analysis to DHFR originated from Chlamydia muridarum and Listeria grayi We found that the acquisiti

30 ce can be successfully infected with both C. muridarum and N. gonorrhoeae and that chlamydia-induced

31 ncoded urogenital pathogenicity factor of C. muridarum and the first with these characteristics to be

32 ong canonical inflammasomes, we find that C. muridarum and the human pathogen Chlamydia trachomatis a

33 infected with the mouse Chlamydia species C. muridarum and then inoculated with N. gonorrhoeae follow

34 culated in the meatus urethra with Chlamydia muridarum and they were caged with naive female mice.

35 susceptible strain of mice (C3H/HeN) with C. muridarum and treated two groups of mice with either one

36 nereum biovars (serovars L1 to L3), (iii) C. muridarum, and (iv) C. pneumoniae and C. caviae.

37 Tarp orthologs from C. pneumoniae, C. muridarum, and C. caviae harbor between 1 and 4 actin bi

38 ecruited to Chlamydia trachomatis, Chlamydia muridarum, and Chlamydia pneumoniae inclusions, whereas

39 tified: Helicobacter hepaticus, Helicobacter muridarum, and Helicobacter bilis.

40 al macrophages were performed with Chlamydia muridarum, and the expression of inflammatory cytokines

41 Chlamydia trachomatis and Chlamydia muridarum are intracellular bacterial pathogens of mucos

42 ttenuated plasmid-cured strains of Chlamydia muridarum are protected from oviduct pathology upon chal

43 nd mice were inoculated intranasally with C. muridarum as positive controls.

44 is may be induced by the gastrointestinal C. muridarum, as a second hit, to transmucosally convert tu

45 gesting that C5 deficiency did not affect C. muridarum ascending infection.

46 nce of serum, H. pylori, H. mustelae, and H. muridarum became sensitive to polymyxin B and/or trimeth

47 A and ihtA from C. trachomatis serovar D, C. muridarum, C. caviae and C. pneumoniae and assayed for r

48 f phosphotyrosine at the site of entry of C. muridarum, C. caviae, and C. pneumoniae, although each s

49 In a Chlamydia muridarum-C57 mouse model, chlamydial organisms are clea

50 infection with Chlamydia trachomatis and C. muridarum can induce long-lasting hydrosalpinx in the up

51 ngly, the mouse-adapted Chlamydia species C. muridarum can infect mice both by transcervical inoculat

52 Orally delivered Chlamydia muridarum can reach the colon and maintain a long-lastin

53 In this study we demonstrate that C. muridarum can specifically evade IRG-mediated host resis

54 t growth of C. muridarum, indicating that C. muridarum can specifically evade Irgb10-driven host resp

55 To test whether hematogenous C. muridarum can spread to and establish a long-lasting col

56 However, gastrointestinal C. muridarum cannot directly autoinoculate the genital trac

57 mmune responses against intranasal Chlamydia muridarum challenge in 1-day-old C57BL/6 and BALB/c mice

58 mediated responses against genital Chlamydia muridarum challenge.

59 Moreover, C. muridarum-challenged HLA-DR4 tg mice exhibited CPAF-spec

60 during infection with the species Chlamydia muridarum, Chlamydia psittaci, and Chlamydia caviae, whi

61 ains an ortholog of Tarp, although Chlamydia muridarum, Chlamydophila caviae, and Chlamydophila pneum

62 ibit suboptimal late phase vaginal Chlamydia muridarum clearance, greater dissemination, and oviduct

63 thepsin-dependent mechanism to facilitate C. muridarum clearance.

64 Il1a(-/-) mice infected with C. muridarum cleared infection at their cervix at the same

65 The mouse-adapted pathogen Chlamydia muridarum (CM) induces pathology in the mouse genital tr

66 Chlamydia muridarum (CM), a model pathogen for investigating CT pa

67 with a plasmid-deficient strain of Chlamydia muridarum, CM3.1, does not induce the development of ovi

68 model combining ovalbumin-induced AAD with C muridarum (Cmu) respiratory infection.

69 Thus, promoting C. muridarum colonization of the gastrointestinal tract may

70 Interestingly, C. muridarum colonization of the gastrointestinal tract pos

71 ion, indicating that pGP3 is critical for C. muridarum colonization of the gastrointestinal tract.

72 amma interferon (IFN-gamma) resistance of C. muridarum compared to C. trachomatis in the murine genit

73 of hydrosalpinx induction by plasmid-free C. muridarum correlated with significantly reduced live org

74 As observed with plasmid-deficient C. muridarum, CTD153 displayed impaired accumulation of gly

75 upper genital tract in mice infected with C. muridarum deficient in Pgp3 but not Pgp7.

76 Unexpectedly, the C. muridarum-derived signal was still detectable in the abd

77 mice intravaginally infected with Chlamydia muridarum developed visible hydrosalpinges in the oviduc

78 l inflammation, we delivered plasmid-free C. muridarum directly into the endometrium by intrauterine

79 Inoculation of C. muridarum directly into the upper genital tract, which r

80 surgical methodology of depositing Chlamydia muridarum directly on the endocervix.

81 e cryptic plasmid is essential for Chlamydia muridarum dissemination from the genital tract to the ga

82 tle as 5 pg of H. hepaticus, H. bilis, or H. muridarum DNA.

83 modulatory cytokine IFN-beta, even though C. muridarum does not have a clear pathogen-associated mole

84 7BL/6 mice with two populations of Chlamydia muridarum, each comprised of multiple genetic variants a

85 were infected intravaginally with Chlamydia muridarum either at zeitgeber time 3, ZT3 and ZT15.

86 mid-free Chlamydia trachomatis and Chlamydia muridarum fail to induce severe pathology.

87 with Helicobacter hepaticus or Helicobacter muridarum, followed by H. pylori infection 2 weeks later

88 ing an oviductal epithelial cell line with C muridarum, followed by immunoaffinity isolation and sequ

89 mice exhibit delayed clearance of Chlamydia muridarum genital infection compared to wild-type (WT) m

90 The murine model of C. muridarum genital infection has been extremely useful fo

91 examined the course and outcome of Chlamydia muridarum genital infection in mice genetically deficien

92 opment of oviduct pathology during Chlamydia muridarum genital infection in the mouse model.

93 Using the Chlamydia muridarum genital infection model of mice, which replica

94 data suggest that type I IFNs exacerbate C. muridarum genital infection through an inhibition of the

95 educed severity of oviduct pathology upon C. muridarum genital infection.

96 macrophage influx or normal resolution of C. muridarum genital infection.

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

98 mately 50% of pre-existing Tregs prior to C. muridarum genital tract infection markedly reduced the f

99 uring system and a murine model of Chlamydia muridarum genital tract infection.

100 ry and sufficient to clear primary Chlamydia muridarum genital tract infections in the mouse model, m

101 ) T cells in resolving C. trachomatis and C. muridarum genital tract infections, we used the female m

102 not compromised in their ability to clear C. muridarum genital tract infections.

103 critical for clearing experimental Chlamydia muridarum genital tract infections.

104 necessary and sufficient to clear Chlamydia muridarum genital tract infections.

105 learance or immunopathology during Chlamydia muridarum genital tract infections.

106 redundant T cell mechanisms for clearing C. muridarum genital tract infections: one dependent on iNO

107 d to C. muridarum inclusions nor restrict C. muridarum growth, we find that GBPs promote inflammasome

108 Although modern Chlamydia muridarum has been passaged for decades, there are no re

109 The mouse chlamydial pathogen Chlamydia muridarum has been used as a model organism for the stud

110 These data suggest that C. muridarum has evolved a mechanism to escape the murine I

111 istinct taxon and clusters with Helicobacter muridarum, Helicobacter hepaticus, and Helicobacter sp.

112 m H. mustelae, H. canis (two strains) and H. muridarum identified insertions of novel sequence (inter

113 e model of genital infection using Chlamydia muridarum, IL-1R signaling plays a critical role in ovid

114 essential role in the development of anti-C. muridarum immunity.

115 t for induction of robust protective anti-C. muridarum immunity.

116 to the host during infection with Chlamydia muridarum in both mouse lung and female genital tract.

117 ibition of host protein synthesis rescued C. muridarum in macrophages infected at a moderate MOI, imp

118 Intravaginal infection with Chlamydia muridarum in mice can ascend to the upper genital tract,

119 While occasional detection of C. suis and C. muridarum in poultry is reported here for the first time

120 el of intracervical infection with Chlamydia muridarum in the mouse to elicit a relatively synchronou

121 Infection with Chlamydia muridarum in the mouse urogenital tract can induce both

122 amined the replicative capacity of Chlamydia muridarum in the RAW 264.7 murine macrophage cell line a

123 Intracellular growth and infectivity of C. muridarum in vitro remain unaffected in the absence of T

124 ed mouse macrophages infected with Chlamydia muridarum in vitro secrete minimal IL-1beta, in vitro pr

125 It has previously been suggested that C. muridarum inactivates the IRG protein Irga6 (Iigp1) to d

126 Although GBPs neither bind to C. muridarum inclusions nor restrict C. muridarum growth, w

127 inclusions but not with C. pneumoniae or C. muridarum inclusions, while the opposite was observed fo

128 We found no evidence that C. muridarum increases gonococcal adherence to, or invasion

129 achomatis but fails to restrict growth of C. muridarum, indicating that C. muridarum can specifically

130 These observations together suggest that C. muridarum-induced protective immunity and inflammatory p

131 mid-competent but not plasmid-free Chlamydia muridarum induces hydrosalpinx in mouse upper genital tr

132 These results indicate that C. muridarum induces IFN-beta via stimulation of nucleotide

133 sponses failed to significantly alter the C. muridarum induction of uterine horn dilation.

134 Also, C. muridarum-infected females delivered significantly fewer

135 The addition of iron to INP0007-treated C. muridarum-infected macrophages not only restored chlamyd

136 is not required for IFN-beta synthesis in C. muridarum-infected macrophages, suggesting that there ar

137 t GBPs promote inflammasome activation in C. muridarum-infected macrophages.

138 More females mated with C. muridarum-infected male mice (35%) than females mated wi

139 or necrosis factor alpha were detected in C. muridarum-infected mice prior to inoculation with N. gon

140 spite the delayed clearance, rechallenged C. muridarum-infected mice were highly immune.

141 C. muridarum-infected murine oviduct epithelial cells secre

142 for secretion of acute phase cytokines by C. muridarum-infected oviduct epithelial cell lines.

143 e of CD8(+) T cells during genital Chlamydia muridarum infection and oviduct sequelae.

144 ce of primary or secondary genital Chlamydia muridarum infection but significantly reduced oviduct pa

145 rotective immunity against genital Chlamydia muridarum infection in BALB/c mice.

146 Here, we utilized in vivo imaging of C. muridarum infection in mice following an intravaginal in

147 salpinx, which can be modeled with Chlamydia muridarum infection in mice.

148 Further, C. muridarum infection induces IFN-beta synthesis in the ov

149 ly convert tubal repairing - initiated by C. muridarum infection of tubal epithelial cells (serving a

150 to show that the IFN-beta secreted during C. muridarum infection requires a functional TLR3.

151 mice for uterine horn dilation following C. muridarum infection revealed that B10.D2, C57BL/10J, and

152 Remarkably, C. muridarum infection subverted the immune suppressive rol

153 Hydrosalpinx induction in mice by Chlamydia muridarum infection, a model that has been used to study

154 to develop robust hydrosalpinx following C. muridarum infection, both contradicting the observation

155 In contrast to C. muridarum infection, C. trachomatis infection was unalte

156 tive immunity to re-challenge, but unlike C. muridarum infection, optimum resistance required multipl

157 The second is the murine model of Chlamydia muridarum infection, which established the essential rol

158 es of wild-type mice early during genital C. muridarum infection, while Th1 cells predominated later.

159 ole in the downstream immune responses to C. muridarum infection.

160 uct pathology during mouse genital Chlamydia muridarum infection.

161 ligand (CD40L)-mediated costimulation in C. muridarum infection.

162 on is not required for protection against C. muridarum infection.

163 ls in protective immunity against genital C. muridarum infection.

164 nd Nod2 in epithelial responses to Chlamydia muridarum infection.

165 detected microscopically following Chlamydia muridarum infection.

166 mpared plasmid-competent and plasmid-free C. muridarum infections in 5 different strains of mice.

167 We demonstrate that C. muridarum infections induce GBP-dependent pyroptosis thr

168 All C. muridarum-inoculated male mice had positive urine cultur

169 mined by serology, all females caged with C. muridarum-inoculated males became infected, and 93% of t

170 We have demonstrated that intravenous C. muridarum inoculation can result in colonization of the

171 Following C. muridarum inoculation, wild-type mice develop robust hyd

172 Direct delivery of C. muridarum into the mouse uterus increased both uterine h

173 e obligate intracellular bacterium Chlamydia muridarum is commonly used as a model for ascending Chla

174 inclusions, remain free of GBPs and that C. muridarum is impervious to GBP-mediated restrictions on

175 To date, two commonly used C. muridarum isolates have been used interchangeably and ar

176 s genotypic and virulence diversity among C. muridarum isolates.

177 ss, and pathological changes after Chlamydia muridarum lung infection compared with wild-type (WT) mi

178 udies have shown immunization with Chlamydia muridarum major outer membrane protein (MOMP) can induce

179 le mice were first vaccinated with Chlamydia muridarum major outer membrane protein (MOMP) plus the a

180 and shortened infection with plasmid-free C. muridarum may contribute significantly to its attenuated

181 H. muridarum-mediated attenuation of gastritis in coinfecte

182 Using the Chlamydia muridarum model of genital infection, we demonstrate a p

183 fection and vaccine development using the C. muridarum model.

184 e manner in which the inoculating dose of C. muridarum modulates a genital infection, we measured inn

185 contrast to L2, the mouse pathogen Chlamydia muridarum (MoPn) was consistently inhibited by BafA in a

186 in from the mouse-specific species Chlamydia muridarum (MoPn-MOMP or mMOMP).

187 Using the C. muridarum mouse infection model, we show that intestinal

188 Studies utilizing the Chlamydia muridarum mouse model have shown that CD4 T cells are cr

189 colonization ability of a pGP3-deficient C. muridarum mutant, suggesting that pGP3 is required for C

190 the results of studies with plasmid-cured C. muridarum mutants that retain the ability to infect the

191 Finally, defective spreading of C. muridarum mutants was due to their inability to colonize

192 C. muridarum mutants, despite their ability to activate acu

193 cine, mice were immunized with the Chlamydia muridarum native major outer membrane protein (nMOMP) so

194 C. muridarum Nigg also effectively competed with CM972 duri

195 t pathology upon challenge with wild-type C. muridarum Nigg despite induction of a response that did

196 -deficient CM972 versus that of wild-type C. muridarum Nigg in mixed inocula in vitro and in vivo.

197 ns correlated directly with the amount of C. muridarum Nigg in the initial inoculum, confirming the r

198 The C. muridarum Weiss isolate and C. muridarum Nigg isolate varied significantly in their vir

199 C. muridarum Nigg rapidly out-competed its plasmid-cured de

200 ation of the CBA/J mice with plasmid-free C. muridarum not only resulted in more infection in the ovi

201 (p.i.), mice immunized with the rMOMP of C. muridarum or C. trachomatis D, E, or F had lost 4%, 6%,

202 iduct epithelial cell lines infected with C. muridarum or exposed to the TLR2 agonist peptidoglycan s

203 lated per os with H. hepaticus, Helicobacter muridarum, or H. bilis.

204 Furthermore, plasmid-competent C. muridarum organisms after UV inactivation were no longer

205 A retro-orbital vein inoculation of the C. muridarum organisms at a lower dose in a different mouse

206 The plasmid-free C. muridarum organisms failed to induce hydrosalpinx even w

207 The C. muridarum organisms spreading from the genital to the GI

208 The Pgp3-deficient C. muridarum organisms were also less invasive when deliver

209 duction than C5(+/+) mice, even when live C. muridarum organisms were directly delivered into the upp

210 Detailed genetic analysis of C. muridarum passages revealed a truncated variant with a G

211 nd represents a major virulence factor in C. muridarum pathogenesis in mice.

212 may be responsible for the attenuation in C. muridarum pathogenicity described above.

213 Nevertheless, C. muridarum Pgp5 is more potent than C. trachomatis Pgp5 i

214 Replacing C. muridarum pgp5 with a C. trachomatis pgp5 still inhibite

215 lation into mice compared to the parental C. muridarum population, CMG0.

216 Of the newborn mice, 32% were C. muridarum positive either in the lungs or in the intesti

217 ositive vaginal swab specimen cultures or C. muridarum-positive pups.

218 owed that DCs infected by C trachomatis or C muridarum present epitopes from a limited spectrum of ch

219 iduct epithelial cells infected by Chlamydia muridarum produced a broad spectrum of chemokines, inclu

220 infection of the vaginal epithelium with C. muridarum produced infections of a duration longer than

221 Mice vaginally infected with C. muridarum produced serum and vaginal wash antibodies and

222 C. muridarum productively infected these macrophages at low

223 first direct evidence that enhanced anti-C. muridarum protective immunity induced by Ag-specific CD4

224 rosalpinges preferentially recognized two C. muridarum proteins (TC0582 and TC0912, designated pathol

225 rom the 40 mice recognized 130 out of 257 C. muridarum proteins as antigens and 17 as immunodominant

226 unity and neutrophil influx during Chlamydia muridarum pulmonary infection, but its role during C. mu

227 Our results suggest that C. muridarum PZ genes are transcribed--and some may produce

228 we isolated and characterized a series of C. muridarum PZ nonsense mutants.

229 cts of BALB/c mice infected with doses of C. muridarum ranging from 10(4) to 10(7) inclusion-forming

230 We found that C. muridarum readily colonized and infected vaginal squamou

231 Intravaginal inoculation with C. muridarum readily induces fibrotic blockage or hydrosalp

232 ific CD4 T cell clone was able to inhibit C. muridarum replication in vitro via induction of epitheli

233 s was not likely critical for controlling C. muridarum replication.

234 e found that transcervical infection with C. muridarum results in higher bacterial burdens in the upp

235 emonstrated that plasmid-deficient Chlamydia muridarum retains the ability to infect the murine genit

236 red from the lungs of mice immunized with C. muridarum rMOMP was 0.13 x 10(6).

237 nereum (LGV) and the murine strain Chlamydia muridarum share 99% of their gene content.

238 PVs formed by the rodent pathogen Chlamydia muridarum, so-called inclusions, remain free of GBPs and

239 not IgG1, and elevated levels of splenic C. muridarum-specific IFN-gamma, not IL-4, production.

240 on in the genital tract, since attenuated C. muridarum spread significantly less to the gastrointesti

241 further confirmed the correlation between C. muridarum spreading to the gastrointestinal tract and it

242 We have recently shown that Chlamydia muridarum spreads from the genital tract to the gastroin

243 ve previously shown that wild-type Chlamydia muridarum spreads to and establishes stable colonization

244 ntravenously with a luciferase-expressing C. muridarum strain and monitored its distribution.

245 Following intravaginal inoculation, a C. muridarum strain deficient in plasmid-encoded pGP3 or pG

246 nally infected with the same plasmid-free C. muridarum strain displayed reduced ascending infection a

247 /Cx), E (Bour), or F (IC-Cal-3) or Chlamydia muridarum strain Nigg II using CpG-1826 and Montanide IS

248 similarly controlled in plasmid-deficient C. muridarum strains CM972 and CM3.1 and plasmid-deficient

249 pGP3-deficient C. muridarum strains did not induce hydrosalpinx or spread

250 53, it was unaltered in plasmid-deficient C. muridarum strains.

251 that plasmid-encoded Pgp3 is required for C. muridarum survival in the mouse genital tract and repres

252 deficiency in pGP3 significantly reduced C. muridarum survival in the mouse vagina and increased C.

253 urvival in the mouse vagina and increased C. muridarum susceptibility to vaginal killing by ~8 times.

254 e infected at ZT3 shed significantly more C. muridarum than mice infected at ZT15.

255 much more similar to orthologs in Chlamydia muridarum than those in the phylogenetically closest spe

256 and T cell depletion studies using Chlamydia muridarum that MHC class II and CD4 T cells are critical

257 nce a similar phenotype was observed with C. muridarum Time course experiments showed that the number

258 rine model of genital disease with Chlamydia muridarum, TLR2 plays a role in both early production of

259 inhibitor, the ability of pGP3-deficient C. muridarum to colonize the gastrointestinal tract was res

260 virulence factor, is essential for Chlamydia muridarum to colonize the mouse gastrointestinal tract.

261 as TNFalpha and IL-13, are essential for C. muridarum to induce tubal fibrosis; this may be induced

262 ant, suggesting that pGP3 is required for C. muridarum to reach but not to colonize the large intesti

263 inal tract, suggesting that the spread of C. muridarum to the gastrointestinal tract may contribute t

264 ded pathogenic determinants, we evaluated C. muridarum transformants deficient in the plasmid-borne g

265 C. muridarum transformants with an in-frame deletion of eit

266 We have developed a C. muridarum transformation system and confirmed Pgp1, -2,

267 a novel function of Pgp5 and developed a C. muridarum transformation system for further mapping chla

268 aling pathways, was evaluated in a Chlamydia muridarum urogenital tract infection model.

269 on of matrix metalloproteinases in Chlamydia muridarum urogenital tract infection of female mice.

270 polymorphisms were identified in a Chlamydia muridarum variant resistant to benzylidene acylhydrazide

271 The pGP3-deficient C. muridarum was more susceptible to lactic acid killing, a

272 The C. muridarum Weiss isolate and C. muridarum Nigg isolate va

273 chomatis L2, serovar B, and serovar D and C. muridarum were all equally susceptible to perforin-2-med

274 usion-forming units (IFU) of plasmid-free C. muridarum were intrauterinally inoculated.

275 lamydia trachomatis serovar L2 and Chlamydia muridarum, which do not express FtsZ, undergo polarized

276 Chlamydia muridarum, which naturally infects mice, can induce hydr

277 a rapid but transient oviduct invasion by C. muridarum with a peak infection on day 7.

278 However, C. muridarum with mutations in chromosomal genes tc0237 and

279 In the present study, we found that C. muridarum with mutations in chromosomal genes tc0237 and

280 ice would affect host responses to Chlamydia muridarum within the reproductive tract.