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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                                          All C. muridarum-inoculated male mice had positive urine cul
14                                        Also, C. muridarum-infected females delivered significantly fe
15 e is genotypic and virulence diversity among C. muridarum isolates.
16 ressed by the animal pathogens C. caviae and C. muridarum.
17 trachomatis L2, serovar B, and serovar D and C. muridarum were all equally susceptible to perforin-2-
18           The C. muridarum Weiss isolate and C. muridarum Nigg isolate varied significantly in their
19    While occasional detection of C. suis and C. muridarum in poultry is reported here for the first t
20 act infection with Chlamydia trachomatis and C. muridarum can induce long-lasting hydrosalpinx in the
21 4(+) T cells in resolving C. trachomatis and C. muridarum genital tract infections, we used the femal
22 with plasmid loss in both C. trachomatis and C. muridarum.
23 the first direct evidence that enhanced anti-C. muridarum protective immunity induced by Ag-specific
24 an essential role in the development of anti-C. muridarum immunity.
25 ient for induction of robust protective anti-C. muridarum immunity.
26 ction in the genital tract, since attenuated C. muridarum spread significantly less to the gastrointe
27 on further confirmed the correlation between C. muridarum spreading to the gastrointestinal tract and
28  mice can be successfully infected with both C. muridarum and N. gonorrhoeae and that chlamydia-induc
29 le for secretion of acute phase cytokines by C. muridarum-infected oviduct epithelial cell lines.
30 atis but is absent from inclusions formed by C. muridarum.
31 to induction of long-lasting hydrosalpinx by C. muridarum.
32 sally convert tubal repairing - initiated by C. muridarum infection of tubal epithelial cells (servin
33 th a rapid but transient oviduct invasion by C. muridarum with a peak infection on day 7.
34 re not compromised in their ability to clear C. muridarum genital tract infections.
35 and redundant T cell mechanisms for clearing C. muridarum genital tract infections: one dependent on
36               Furthermore, plasmid-competent C. muridarum organisms after UV inactivation were no lon
37 ysis was not likely critical for controlling C. muridarum replication.
38 rt the results of studies with plasmid-cured C. muridarum mutants that retain the ability to infect t
39 hctA and ihtA from C. trachomatis serovar D, C. muridarum, C. caviae and C. pneumoniae and assayed fo
40 the colonization ability of a pGP3-deficient C. muridarum mutant, suggesting that pGP3 is required fo
41                           The Pgp3-deficient C. muridarum organisms were also less invasive when deli
42                               pGP3-deficient C. muridarum strains did not induce hydrosalpinx or spre
43 ump inhibitor, the ability of pGP3-deficient C. muridarum to colonize the gastrointestinal tract was
44                           The pGP3-deficient C. muridarum was more susceptible to lactic acid killing
45 as similarly controlled in plasmid-deficient C. muridarum strains CM972 and CM3.1 and plasmid-deficie
46 TD153, it was unaltered in plasmid-deficient C. muridarum strains.
47           As observed with plasmid-deficient C. muridarum, CTD153 displayed impaired accumulation of
48 rum pulmonary infection, but its role during C. muridarum genital tract infection has not been descri
49 ls to show that the IFN-beta secreted during C. muridarum infection requires a functional TLR3.
50 ncoded pathogenic determinants, we evaluated C. muridarum transformants deficient in the plasmid-born
51 ese data suggest that type I IFNs exacerbate C. muridarum genital infection through an inhibition of
52 e intravenously with a luciferase-expressing C. muridarum strain and monitored its distribution.
53  cathepsin-dependent mechanism to facilitate C. muridarum clearance.
54                                    Following C. muridarum inoculation, wild-type mice develop robust
55  of mice for uterine horn dilation following C. muridarum infection revealed that B10.D2, C57BL/10J,
56 ble to develop robust hydrosalpinx following C. muridarum infection, both contradicting the observati
57 ession, indicating that pGP3 is critical for C. muridarum colonization of the gastrointestinal tract.
58 uch as TNFalpha and IL-13, are essential for C. muridarum to induce tubal fibrosis; this may be induc
59 te that plasmid-encoded Pgp3 is required for C. muridarum survival in the mouse genital tract and rep
60 mutant, suggesting that pGP3 is required for C. muridarum to reach but not to colonize the large inte
61  by intrauterine infection with plasmid-free C. muridarum a suitable model for investigating plasmid-
62 ck of hydrosalpinx induction by plasmid-free C. muridarum correlated with significantly reduced live
63 ubal inflammation, we delivered plasmid-free C. muridarum directly into the endometrium by intrauteri
64  compared plasmid-competent and plasmid-free C. muridarum infections in 5 different strains of mice.
65 of and shortened infection with plasmid-free C. muridarum may contribute significantly to its attenua
66 culation of the CBA/J mice with plasmid-free C. muridarum not only resulted in more infection in the
67                             The plasmid-free C. muridarum organisms failed to induce hydrosalpinx eve
68 aginally infected with the same plasmid-free C. muridarum strain displayed reduced ascending infectio
69 nclusion-forming units (IFU) of plasmid-free C. muridarum were intrauterinally inoculated.
70 tent, but not inoculation with plasmid-free, C. muridarum.
71                                     Further, C. muridarum infection induces IFN-beta synthesis in the
72                    However, gastrointestinal C. muridarum cannot directly autoinoculate the genital t
73  this may be induced by the gastrointestinal C. muridarum, as a second hit, to transmucosally convert
74 cells in protective immunity against genital C. muridarum infection.
75 nodes of wild-type mice early during genital C. muridarum infection, while Th1 cells predominated lat
76                 To test whether hematogenous C. muridarum can spread to and establish a long-lasting
77                                     However, C. muridarum with mutations in chromosomal genes tc0237
78  venereum biovars (serovars L1 to L3), (iii) C. muridarum, and (iv) C. pneumoniae and C. caviae.
79 that GBPs promote inflammasome activation in C. muridarum-infected macrophages.
80 p3 may be responsible for the attenuation in C. muridarum pathogenicity described above.
81 D40 ligand (CD40L)-mediated costimulation in C. muridarum infection.
82 tumor necrosis factor alpha were detected in C. muridarum-infected mice prior to inoculation with N.
83 t and represents a major virulence factor in C. muridarum pathogenesis in mice.
84 ay is not required for IFN-beta synthesis in C. muridarum-infected macrophages, suggesting that there
85 m survival in the mouse vagina and increased C. muridarum susceptibility to vaginal killing by ~8 tim
86 pecific CD4 T cell clone was able to inhibit C. muridarum replication in vitro via induction of epith
87                               Interestingly, C. muridarum colonization of the gastrointestinal tract
88        We have demonstrated that intravenous C. muridarum inoculation can result in colonization of t
89  induction than C5(+/+) mice, even when live C. muridarum organisms were directly delivered into the
90 Mice infected at ZT3 shed significantly more C. muridarum than mice infected at ZT15.
91                                    Moreover, C. muridarum-challenged HLA-DR4 tg mice exhibited CPAF-s
92                                Nevertheless, C. muridarum Pgp5 is more potent than C. trachomatis Pgp
93 tions correlated directly with the amount of C. muridarum Nigg in the initial inoculum, confirming th
94                 Detailed genetic analysis of C. muridarum passages revealed a truncated variant with
95                           Direct delivery of C. muridarum into the mouse uterus increased both uterin
96  the manner in which the inoculating dose of C. muridarum modulates a genital infection, we measured
97 tracts of BALB/c mice infected with doses of C. muridarum ranging from 10(4) to 10(7) inclusion-formi
98 e of phosphotyrosine at the site of entry of C. muridarum, C. caviae, and C. pneumoniae, although eac
99 e-encoded urogenital pathogenicity factor of C. muridarum and the first with these characteristics to
100  trachomatis but fails to restrict growth of C. muridarum, indicating that C. muridarum can specifica
101  with 10(4) inclusion-forming units (IFU) of C. muridarum.
102         Here, we utilized in vivo imaging of C. muridarum infection in mice following an intravaginal
103      Intracellular growth and infectivity of C. muridarum in vitro remain unaffected in the absence o
104                               Inoculation of C. muridarum directly into the upper genital tract, whic
105                          The murine model of C. muridarum genital infection has been extremely useful
106 d gamma interferon (IFN-gamma) resistance of C. muridarum compared to C. trachomatis in the murine ge
107 or macrophage influx or normal resolution of C. muridarum genital infection.
108 ion (p.i.), mice immunized with the rMOMP of C. muridarum or C. trachomatis D, E, or F had lost 4%, 6
109 s, we isolated and characterized a series of C. muridarum PZ nonsense mutants.
110 estinal tract, suggesting that the spread of C. muridarum to the gastrointestinal tract may contribut
111              Finally, defective spreading of C. muridarum mutants was due to their inability to colon
112 o positive vaginal swab specimen cultures or C. muridarum-positive pups.
113 tis inclusions but not with C. pneumoniae or C. muridarum inclusions, while the opposite was observed
114 oculation into mice compared to the parental C. muridarum population, CMG0.
115           Tarp orthologs from C. pneumoniae, C. muridarum, and C. caviae harbor between 1 and 4 actin
116                              Thus, promoting C. muridarum colonization of the gastrointestinal tract
117  Despite the delayed clearance, rechallenged C. muridarum-infected mice were highly immune.
118 ct, deficiency in pGP3 significantly reduced C. muridarum survival in the mouse vagina and increased
119                                  Remarkably, C. muridarum infection subverted the immune suppressive
120                                    Replacing C. muridarum pgp5 with a C. trachomatis pgp5 still inhib
121 Inhibition of host protein synthesis rescued C. muridarum in macrophages infected at a moderate MOI,
122 bind to C. muridarum inclusions nor restrict C. muridarum growth, we find that GBPs promote inflammas
123 st infected with the mouse Chlamydia species C. muridarum and then inoculated with N. gonorrhoeae fol
124 stingly, the mouse-adapted Chlamydia species C. muridarum can infect mice both by transcervical inocu
125 2b, not IgG1, and elevated levels of splenic C. muridarum-specific IFN-gamma, not IL-4, production.
126 led inclusions, remain free of GBPs and that C. muridarum is impervious to GBP-mediated restrictions
127            In this study we demonstrate that C. muridarum can specifically evade IRG-mediated host re
128                          We demonstrate that C. muridarum infections induce GBP-dependent pyroptosis
129                    We found no evidence that C. muridarum increases gonococcal adherence to, or invas
130  Among canonical inflammasomes, we find that C. muridarum and the human pathogen Chlamydia trachomati
131                                We found that C. muridarum readily colonized and infected vaginal squa
132          In the present study, we found that C. muridarum with mutations in chromosomal genes tc0237
133                  These results indicate that C. muridarum induces IFN-beta via stimulation of nucleot
134 rict growth of C. muridarum, indicating that C. muridarum can specifically evade Irgb10-driven host r
135                      These data suggest that C. muridarum has evolved a mechanism to escape the murin
136                     Our results suggest that C. muridarum PZ genes are transcribed--and some may prod
137     These observations together suggest that C. muridarum-induced protective immunity and inflammator
138        It has previously been suggested that C. muridarum inactivates the IRG protein Irga6 (Iigp1) t
139                                          The C. muridarum organisms spreading from the genital to the
140                                          The C. muridarum Weiss isolate and C. muridarum Nigg isolate
141  responses failed to significantly alter the C. muridarum induction of uterine horn dilation.
142      A retro-orbital vein inoculation of the C. muridarum organisms at a lower dose in a different mo
143                            Unexpectedly, the C. muridarum-derived signal was still detectable in the
144  infection and vaccine development using the C. muridarum model.
145                                    Using the C. muridarum mouse infection model, we show that intesti
146 unomodulatory cytokine IFN-beta, even though C. muridarum does not have a clear pathogen-associated m
147                Although GBPs neither bind to C. muridarum inclusions nor restrict C. muridarum growth
148                               In contrast to C. muridarum infection, C. trachomatis infection was una
149 duce genomic and phenotypic perturbations to C. muridarum, a starter population was passaged in cultu
150 oximately 50% of pre-existing Tregs prior to C. muridarum genital tract infection markedly reduced th
151 a role in the downstream immune responses to C. muridarum infection.
152      The addition of iron to INP0007-treated C. muridarum-infected macrophages not only restored chla
153 hydrosalpinges preferentially recognized two C. muridarum proteins (TC0582 and TC0912, designated pat
154 duct pathology upon challenge with wild-type C. muridarum Nigg despite induction of a response that d
155 mid-deficient CM972 versus that of wild-type C. muridarum Nigg in mixed inocula in vitro and in vivo.
156 tective immunity to re-challenge, but unlike C. muridarum infection, optimum resistance required mult
157 d reduced severity of oviduct pathology upon C. muridarum genital infection.
158                   To date, two commonly used C. muridarum isolates have been used interchangeably and
159 oviduct disease upon challenge with virulent C. muridarum.
160                Of the newborn mice, 32% were C. muridarum positive either in the lungs or in the inte
161 termined by serology, all females caged with C. muridarum-inoculated males became infected, and 93% o
162 nide ISA 720; then they were challenged with C. muridarum.
163 ary infection of the vaginal epithelium with C. muridarum produced infections of a duration longer th
164  a susceptible strain of mice (C3H/HeN) with C. muridarum and treated two groups of mice with either
165 overed from the lungs of mice immunized with C. muridarum rMOMP was 0.13 x 10(6).
166                 Il1a(-/-) mice infected with C. muridarum cleared infection at their cervix at the sa
167 he upper genital tract in mice infected with C. muridarum deficient in Pgp3 but not Pgp7.
168  Oviduct epithelial cell lines infected with C. muridarum or exposed to the TLR2 agonist peptidoglyca
169                 Mice vaginally infected with C. muridarum produced serum and vaginal wash antibodies
170   We found that transcervical infection with C. muridarum results in higher bacterial burdens in the
171                Intravaginal inoculation with C. muridarum readily induces fibrotic blockage or hydros
172 , and mice were inoculated intranasally with C. muridarum as positive controls.
173  animals were challenged intravaginally with C. muridarum.
174 n vitro infection of primed macrophages with C. muridarum.
175                      More females mated with C. muridarum-infected male mice (35%) than females mated
176  since a similar phenotype was observed with C. muridarum Time course experiments showed that the num
177  T cells, and then challenged vaginally with C. muridarum.

 
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