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1 did so following intravaginal infection with Chlamydia muridarum.
2 arized division of Chlamydia trachomatis and Chlamydia muridarum.
3 ion with the obligate intracellular pathogen Chlamydia muridarum.
4 growth of the closely related mouse pathogen Chlamydia muridarum.
5 7BL/6 mice were infected intravaginally with Chlamydia muridarum.
6  in the genital tracts of mice infected with Chlamydia muridarum, a model for investigating the human
7                                              Chlamydia muridarum, a model pathogen for investigating
8  the tc0668 gene of serial in vitro-passaged Chlamydia muridarum, a murine model of human urogenital
9 cular serovars of C. trachomatis, as well as Chlamydia muridarum and Chlamydia caviae.
10                   The native plasmid of both Chlamydia muridarum and Chlamydia trachomatis has been s
11                                              Chlamydia muridarum and Chlamydia trachomatis mouse mode
12 munity of hysterectomized mice infected with Chlamydia muridarum and Chlamydia trachomatis to determi
13 h CD4 T cells that respond to a common Ag in Chlamydia muridarum and Chlamydia trachomatis Using an a
14 tended this analysis to DHFR originated from Chlamydia muridarum and Listeria grayi We found that the
15 e were inoculated in the meatus urethra with Chlamydia muridarum and they were caged with naive femal
16 ing, are recruited to Chlamydia trachomatis, Chlamydia muridarum, and Chlamydia pneumoniae inclusions
17 e peritoneal macrophages were performed with Chlamydia muridarum, and the expression of inflammatory
18                    Chlamydia trachomatis and Chlamydia muridarum are intracellular bacterial pathogen
19 ted with attenuated plasmid-cured strains of Chlamydia muridarum are protected from oviduct pathology
20                                         In a Chlamydia muridarum-C57 mouse model, chlamydial organism
21                             Orally delivered Chlamydia muridarum can reach the colon and maintain a l
22 otective immune responses against intranasal Chlamydia muridarum challenge in 1-day-old C57BL/6 and B
23  and CPAF-mediated responses against genital Chlamydia muridarum challenge.
24 o produced during infection with the species Chlamydia muridarum, Chlamydia psittaci, and Chlamydia c
25  each contains an ortholog of Tarp, although Chlamydia muridarum, Chlamydophila caviae, and Chlamydop
26 t mice exhibit suboptimal late phase vaginal Chlamydia muridarum clearance, greater dissemination, an
27                   The mouse-adapted pathogen Chlamydia muridarum (CM) induces pathology in the mouse
28                                              Chlamydia muridarum (CM), a model pathogen for investiga
29 n of mice with a plasmid-deficient strain of Chlamydia muridarum, CM3.1, does not induce the developm
30 , 27 of 40 mice intravaginally infected with Chlamydia muridarum developed visible hydrosalpinges in
31 loped the surgical methodology of depositing Chlamydia muridarum directly on the endocervix.
32         The cryptic plasmid is essential for Chlamydia muridarum dissemination from the genital tract
33 nfected C57BL/6 mice with two populations of Chlamydia muridarum, each comprised of multiple genetic
34 (LD) cycle were infected intravaginally with Chlamydia muridarum either at zeitgeber time 3, ZT3 and
35       Plasmid-free Chlamydia trachomatis and Chlamydia muridarum fail to induce severe pathology.
36 ckout (KO) mice exhibit delayed clearance of Chlamydia muridarum genital infection compared to wild-t
37 ction, we examined the course and outcome of Chlamydia muridarum genital infection in mice geneticall
38  the development of oviduct pathology during Chlamydia muridarum genital infection in the mouse model
39                                    Using the Chlamydia muridarum genital infection model of mice, whi
40 tro coculturing system and a murine model of Chlamydia muridarum genital tract infection.
41 re necessary and sufficient to clear primary Chlamydia muridarum genital tract infections in the mous
42 acterial clearance or immunopathology during Chlamydia muridarum genital tract infections.
43 cells are critical for clearing experimental Chlamydia muridarum genital tract infections.
44  cells are necessary and sufficient to clear Chlamydia muridarum genital tract infections.
45                              Although modern Chlamydia muridarum has been passaged for decades, there
46                The mouse chlamydial pathogen Chlamydia muridarum has been used as a model organism fo
47 n the mouse model of genital infection using Chlamydia muridarum, IL-1R signaling plays a critical ro
48 etrimental to the host during infection with Chlamydia muridarum in both mouse lung and female genita
49                  Intravaginal infection with Chlamydia muridarum in mice can ascend to the upper geni
50 eloped model of intracervical infection with Chlamydia muridarum in the mouse to elicit a relatively
51                               Infection with Chlamydia muridarum in the mouse urogenital tract can in
52 udy, we examined the replicative capacity of Chlamydia muridarum in the RAW 264.7 murine macrophage c
53 ugh elicited mouse macrophages infected with Chlamydia muridarum in vitro secrete minimal IL-1beta, i
54  with plasmid-competent but not plasmid-free Chlamydia muridarum induces hydrosalpinx in mouse upper
55 ed the role of CD8(+) T cells during genital Chlamydia muridarum infection and oviduct sequelae.
56 le clearance of primary or secondary genital Chlamydia muridarum infection but significantly reduced
57 sess the protective immunity against genital Chlamydia muridarum infection in BALB/c mice.
58 h as hydrosalpinx, which can be modeled with Chlamydia muridarum infection in mice.
59            Hydrosalpinx induction in mice by Chlamydia muridarum infection, a model that has been use
60            The second is the murine model of Chlamydia muridarum infection, which established the ess
61 es to oviduct pathology during mouse genital Chlamydia muridarum infection.
62  dilation detected microscopically following Chlamydia muridarum infection.
63 ins Nod1 and Nod2 in epithelial responses to Chlamydia muridarum infection.
64 on with the obligate intracellular bacterium Chlamydia muridarum is commonly used as a model for asce
65  weight loss, and pathological changes after Chlamydia muridarum lung infection compared with wild-ty
66       Female mice were first vaccinated with Chlamydia muridarum major outer membrane protein (MOMP)
67  Recent studies have shown immunization with Chlamydia muridarum major outer membrane protein (MOMP)
68                                    Using the Chlamydia muridarum model of genital infection, we demon
69        In contrast to L2, the mouse pathogen Chlamydia muridarum (MoPn) was consistently inhibited by
70 MOMP protein from the mouse-specific species Chlamydia muridarum (MoPn-MOMP or mMOMP).
71                        Studies utilizing the Chlamydia muridarum mouse model have shown that CD4 T ce
72  a new vaccine, mice were immunized with the Chlamydia muridarum native major outer membrane protein
73 pected, oviduct epithelial cells infected by Chlamydia muridarum produced a broad spectrum of chemoki
74 of Th1 immunity and neutrophil influx during Chlamydia muridarum pulmonary infection, but its role du
75 eviously demonstrated that plasmid-deficient Chlamydia muridarum retains the ability to infect the mu
76 anuloma venereum (LGV) and the murine strain Chlamydia muridarum share 99% of their gene content.
77  show that PVs formed by the rodent pathogen Chlamydia muridarum, so-called inclusions, remain free o
78                  We have recently shown that Chlamydia muridarum spreads from the genital tract to th
79      We have previously shown that wild-type Chlamydia muridarum spreads to and establishes stable co
80 rs D (UW-3/Cx), E (Bour), or F (IC-Cal-3) or Chlamydia muridarum strain Nigg II using CpG-1826 and Mo
81 the RTR is much more similar to orthologs in Chlamydia muridarum than those in the phylogenetically c
82 kout mice and T cell depletion studies using Chlamydia muridarum that MHC class II and CD4 T cells ar
83  In the murine model of genital disease with Chlamydia muridarum, TLR2 plays a role in both early pro
84 tal tract virulence factor, is essential for Chlamydia muridarum to colonize the mouse gastrointestin
85 vated signaling pathways, was evaluated in a Chlamydia muridarum urogenital tract infection model.
86 d expression of matrix metalloproteinases in Chlamydia muridarum urogenital tract infection of female
87 ucleotide polymorphisms were identified in a Chlamydia muridarum variant resistant to benzylidene acy
88         Chlamydia trachomatis serovar L2 and Chlamydia muridarum, which do not express FtsZ, undergo
89                                              Chlamydia muridarum, which naturally infects mice, can i
90 eficient mice would affect host responses to Chlamydia muridarum within the reproductive tract.