ライフサイエンスコーパス: muridarum

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

2 itro infection of primed macrophages with C. muridarum.

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

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

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

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

7 he obligate intracellular pathogen Chlamydia muridarum.

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

9 the closely related mouse pathogen Chlamydia muridarum.

10 duct disease upon challenge with virulent C. muridarum.

11 were infected intravaginally with Chlamydia muridarum.

12 lowing intravaginal infection with Chlamydia muridarum.

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

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

15 imals were challenged intravaginally with C. muridarum.

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

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

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

19 8 gene of serial in vitro-passaged Chlamydia muridarum, a murine model of human urogenital C. trachom

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

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

22 Chlamydia muridarum and Chlamydia trachomatis mouse models of geni

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 mediated responses against genital Chlamydia muridarum challenge.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 7BL/6 mice with two populations of Chlamydia muridarum, each comprised of multiple genetic variants a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 critical for clearing experimental Chlamydia muridarum genital tract infections.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 C. muridarum-infected murine oviduct epithelial cells secre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 nd Nod2 in epithelial responses to Chlamydia muridarum infection.

143 detected microscopically following Chlamydia muridarum infection.

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

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

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

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

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

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

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

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

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

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

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

155 H. muridarum-mediated attenuation of gastritis in coinfecte

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

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

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

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

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

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

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

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

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

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

166 C. muridarum Nigg also effectively competed with CM972 duri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 C. muridarum productively infected these macrophages at low

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 53, it was unaltered in plasmid-deficient C. muridarum strains.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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