ライフサイエンスコーパス: C. muridarum

1 C. muridarum mutants, despite their ability to activate

2 C. muridarum Nigg also effectively competed with CM972 d

3 C. muridarum Nigg rapidly out-competed its plasmid-cured

4 C. muridarum productively infected these macrophages at

5 C. muridarum transformants with an in-frame deletion of

6 C. muridarum-infected murine oviduct epithelial cells se

7 a from the 40 mice recognized 130 out of 257 C. muridarum proteins as antigens and 17 as immunodomina

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

9 red a novel function of Pgp5 and developed a C. muridarum transformation system for further mapping c

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

11 suggesting that C5 deficiency did not affect C. muridarum ascending infection.

12 ation is not required for protection against C. muridarum infection.

13 e is genotypic and virulence diversity among C. muridarum isolates.

14 ressed by the animal pathogens C. caviae and C. muridarum.

15 trachomatis L2, serovar B, and serovar D and C. muridarum were all equally susceptible to perforin-2-

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

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

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

19 4(+) T cells in resolving C. trachomatis and C. muridarum genital tract infections, we used the femal

20 with plasmid loss in both C. trachomatis and C. muridarum.

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

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

23 ient for induction of robust protective anti-C. muridarum immunity.

24 ction in the genital tract, since attenuated C. muridarum spread significantly less to the gastrointe

25 on further confirmed the correlation between C. muridarum spreading to the gastrointestinal tract and

26 mice can be successfully infected with both C. muridarum and N. gonorrhoeae and that chlamydia-induc

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

28 atis but is absent from inclusions formed by C. muridarum.

29 to induction of long-lasting hydrosalpinx by C. muridarum.

30 sally convert tubal repairing - initiated by C. muridarum infection of tubal epithelial cells (servin

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

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

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

34 Furthermore, plasmid-competent C. muridarum organisms after UV inactivation were no lon

35 ysis was not likely critical for controlling C. muridarum replication.

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

37 hctA and ihtA from C. trachomatis serovar D, C. muridarum, C. caviae and C. pneumoniae and assayed fo

38 The Pgp3-deficient C. muridarum organisms were also less invasive when deli

39 pGP3-deficient C. muridarum strains did not induce hydrosalpinx or spre

40 as similarly controlled in plasmid-deficient C. muridarum strains CM972 and CM3.1 and plasmid-deficie

41 TD153, it was unaltered in plasmid-deficient C. muridarum strains.

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

43 rum pulmonary infection, but its role during C. muridarum genital tract infection has not been descri

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

45 ncoded pathogenic determinants, we evaluated C. muridarum transformants deficient in the plasmid-born

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

47 e intravenously with a luciferase-expressing C. muridarum strain and monitored its distribution.

48 cathepsin-dependent mechanism to facilitate C. muridarum clearance.

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

50 ession, indicating that pGP3 is critical for C. muridarum colonization of the gastrointestinal tract.

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

52 te that plasmid-encoded Pgp3 is required for C. muridarum survival in the mouse genital tract and rep

53 by intrauterine infection with plasmid-free C. muridarum a suitable model for investigating plasmid-

54 ck of hydrosalpinx induction by plasmid-free C. muridarum correlated with significantly reduced live

55 ubal inflammation, we delivered plasmid-free C. muridarum directly into the endometrium by intrauteri

56 compared plasmid-competent and plasmid-free C. muridarum infections in 5 different strains of mice.

57 of and shortened infection with plasmid-free C. muridarum may contribute significantly to its attenua

58 culation of the CBA/J mice with plasmid-free C. muridarum not only resulted in more infection in the

59 The plasmid-free C. muridarum organisms failed to induce hydrosalpinx eve

60 aginally infected with the same plasmid-free C. muridarum strain displayed reduced ascending infectio

61 nclusion-forming units (IFU) of plasmid-free C. muridarum were intrauterinally inoculated.

62 tent, but not inoculation with plasmid-free, C. muridarum.

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

64 However, gastrointestinal C. muridarum cannot directly autoinoculate the genital t

65 this may be induced by the gastrointestinal C. muridarum, as a second hit, to transmucosally convert

66 cells in protective immunity against genital C. muridarum infection.

67 nodes of wild-type mice early during genital C. muridarum infection, while Th1 cells predominated lat

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

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

70 that GBPs promote inflammasome activation in C. muridarum-infected macrophages.

71 p3 may be responsible for the attenuation in C. muridarum pathogenicity described above.

72 D40 ligand (CD40L)-mediated costimulation in C. muridarum infection.

73 tumor necrosis factor alpha were detected in C. muridarum-infected mice prior to inoculation with N.

74 t and represents a major virulence factor in C. muridarum pathogenesis in mice.

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

76 pecific CD4 T cell clone was able to inhibit C. muridarum replication in vitro via induction of epith

77 Interestingly, C. muridarum colonization of the gastrointestinal tract

78 We have demonstrated that intravenous C. muridarum inoculation can result in colonization of t

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

80 Moreover, C. muridarum-challenged HLA-DR4 tg mice exhibited CPAF-s

81 Nevertheless, C. muridarum Pgp5 is more potent than C. trachomatis Pgp

82 tions correlated directly with the amount of C. muridarum Nigg in the initial inoculum, confirming th

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

84 Direct delivery of C. muridarum into the mouse uterus increased both uterin

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

86 tracts of BALB/c mice infected with doses of C. muridarum ranging from 10(4) to 10(7) inclusion-formi

87 e of phosphotyrosine at the site of entry of C. muridarum, C. caviae, and C. pneumoniae, although eac

88 e-encoded urogenital pathogenicity factor of C. muridarum and the first with these characteristics to

89 trachomatis but fails to restrict growth of C. muridarum, indicating that C. muridarum can specifica

90 with 10(4) inclusion-forming units (IFU) of C. muridarum.

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

92 Intracellular growth and infectivity of C. muridarum in vitro remain unaffected in the absence o

93 Inoculation of C. muridarum directly into the upper genital tract, whic

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

95 d gamma interferon (IFN-gamma) resistance of C. muridarum compared to C. trachomatis in the murine ge

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

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

98 s, we isolated and characterized a series of C. muridarum PZ nonsense mutants.

99 estinal tract, suggesting that the spread of C. muridarum to the gastrointestinal tract may contribut

100 Finally, defective spreading of C. muridarum mutants was due to their inability to colon

101 tis inclusions but not with C. pneumoniae or C. muridarum inclusions, while the opposite was observed

102 oculation into mice compared to the parental C. muridarum population, CMG0.

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

104 Thus, promoting C. muridarum colonization of the gastrointestinal tract

105 Despite the delayed clearance, rechallenged C. muridarum-infected mice were highly immune.

106 Remarkably, C. muridarum infection subverted the immune suppressive

107 Replacing C. muridarum pgp5 with a C. trachomatis pgp5 still inhib

108 Inhibition of host protein synthesis rescued C. muridarum in macrophages infected at a moderate MOI,

109 bind to C. muridarum inclusions nor restrict C. muridarum growth, we find that GBPs promote inflammas

110 st infected with the mouse Chlamydia species C. muridarum and then inoculated with N. gonorrhoeae fol

111 2b, not IgG1, and elevated levels of splenic C. muridarum-specific IFN-gamma, not IL-4, production.

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

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

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

115 We found no evidence that C. muridarum increases gonococcal adherence to, or invas

116 Among canonical inflammasomes, we find that C. muridarum and the human pathogen Chlamydia trachomati

117 We found that C. muridarum readily colonized and infected vaginal squa

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

119 These results indicate that C. muridarum induces IFN-beta via stimulation of nucleot

120 rict growth of C. muridarum, indicating that C. muridarum can specifically evade Irgb10-driven host r

121 These data suggest that C. muridarum has evolved a mechanism to escape the murin

122 Our results suggest that C. muridarum PZ genes are transcribed--and some may prod

123 These observations together suggest that C. muridarum-induced protective immunity and inflammator

124 It has previously been suggested that C. muridarum inactivates the IRG protein Irga6 (Iigp1) t

125 The C. muridarum organisms spreading from the genital to the

126 The C. muridarum Weiss isolate and C. muridarum Nigg isolate

127 responses failed to significantly alter the C. muridarum induction of uterine horn dilation.

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

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

130 infection and vaccine development using the C. muridarum model.

131 unomodulatory cytokine IFN-beta, even though C. muridarum does not have a clear pathogen-associated m

132 Although GBPs neither bind to C. muridarum inclusions nor restrict C. muridarum growth

133 In contrast to C. muridarum infection, C. trachomatis infection was una

134 duce genomic and phenotypic perturbations to C. muridarum, a starter population was passaged in cultu

135 oximately 50% of pre-existing Tregs prior to C. muridarum genital tract infection markedly reduced th

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

137 hydrosalpinges preferentially recognized two C. muridarum proteins (TC0582 and TC0912, designated pat

138 duct pathology upon challenge with wild-type C. muridarum Nigg despite induction of a response that d

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

140 tective immunity to re-challenge, but unlike C. muridarum infection, optimum resistance required mult

141 d reduced severity of oviduct pathology upon C. muridarum genital infection.

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

143 oviduct disease upon challenge with virulent C. muridarum.

144 nide ISA 720; then they were challenged with C. muridarum.

145 ary infection of the vaginal epithelium with C. muridarum produced infections of a duration longer th

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

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

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

149 Oviduct epithelial cell lines infected with C. muridarum or exposed to the TLR2 agonist peptidoglyca

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

151 , and mice were inoculated intranasally with C. muridarum as positive controls.

152 animals were challenged intravaginally with C. muridarum.

153 n vitro infection of primed macrophages with C. muridarum.

154 T cells, and then challenged vaginally with C. muridarum.