scholarly journals The Duration of Chlamydia muridarum Genital Tract Infection and Associated Chronic Pathological Changes Are Reduced in IL-17 Knockout Mice but Protection Is Not Increased Further by Immunization

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e76664 ◽  
Author(s):  
Dean W. Andrew ◽  
Melanie Cochrane ◽  
Justin H. Schripsema ◽  
Kyle H. Ramsey ◽  
Samantha J. Dando ◽  
...  
Keyword(s):  
Tract Infection ◽  
Knockout Mice ◽  
Genital Tract ◽  
Pathological Changes ◽  
Genital Tract Infection ◽  
Chlamydia Muridarum

scholarly journals Histopathologic Changes Related to Fibrotic Oviduct Occlusion After Genital Tract Infection of Mice With Chlamydia muridarum

2005 ◽  
Vol 32 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Anita A. Shah ◽  
Justin H. Schripsema ◽  
Mohammad T. Imtiaz ◽  
Ira M. Sigar ◽  
John Kasimos ◽  
...  
Keyword(s):  
Tract Infection ◽  
Genital Tract ◽  
Genital Tract Infection ◽  
Chlamydia Muridarum ◽  
Histopathologic Changes

scholarly journals Chlamydia trachomatis genital tract infection of antibody-deficient gene knockout mice.

1997 ◽  
Vol 65 (6) ◽  
pp. 1993-1999 ◽  
Author(s):  
H Su ◽  
K Feilzer ◽  
H D Caldwell ◽  
R P Morrison
Keyword(s):  
Chlamydia Trachomatis ◽  
Tract Infection ◽  
Knockout Mice ◽  
Genital Tract ◽  
Gene Knockout ◽  
Genital Tract Infection ◽  
Gene Knockout Mice

scholarly journals Toll-like receptor 3 (TLR3) promotes the resolution of Chlamydia muridarum genital tract infection in congenic C57BL/6N mice

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195165 ◽  
Author(s):  
Sebastian E. Carrasco ◽  
Sishun Hu ◽  
Denise M. Imai ◽  
Ramesh Kumar ◽  
George E. Sandusky ◽  
...  
Keyword(s):  
Tract Infection ◽  
Genital Tract ◽  
Toll Like Receptor ◽  
Genital Tract Infection ◽  
Chlamydia Muridarum

The role of an enzymatically inactive CPAF mutant vaccination in Chlamydia muridarum genital tract infection

2021 ◽  
pp. 105137
Author(s):  
Hui Chen ◽  
Bo Peng ◽  
Chunfen Yang ◽  
Lijuan Xie ◽  
Shufang Zhong ◽  
...  
Keyword(s):  
Tract Infection ◽  
Genital Tract ◽  
Genital Tract Infection ◽  
Chlamydia Muridarum

Male Rat Genital Tract Infection With Chlamydia Muridarum has No Significant Consequence on Male Fertility

2012 ◽  
Vol 187 (5) ◽  
pp. 1911-1917 ◽  
Author(s):  
Ruben Darío Motrich ◽  
Leonardo Sanchez ◽  
Mariana Maccioni ◽  
Juan Pablo Mackern-Oberti ◽  
Virginia Elena Rivero
Keyword(s):  
Tract Infection ◽  
Genital Tract ◽  
Male Fertility ◽  
Male Rat ◽  
Genital Tract Infection ◽  
Chlamydia Muridarum

scholarly journals CD43−, but not CD43+, IL-10-producing CD1dhiCD5+ B cells suppress type 1 immune responses during Chlamydia muridarum genital tract infection

2014 ◽  
Vol 8 (1) ◽  
pp. 94-106 ◽  
Author(s):  
J M Moore-Connors ◽  
H S Kim ◽  
J S Marshall ◽  
A W Stadnyk ◽  
S A Halperin ◽  
...  
Keyword(s):  
B Cells ◽  
Tract Infection ◽  
Immune Responses ◽  
Genital Tract ◽  
Genital Tract Infection ◽  
Chlamydia Muridarum

Male Rodent Genital Tract Infection With Chlamydia Muridarum: Persistence in the Prostate Gland That Triggers Self-Immune Reactions in Genetically Susceptible Hosts

2011 ◽  
Vol 186 (3) ◽  
pp. 1100-1106 ◽  
Author(s):  
Juan Pablo Mackern-Oberti ◽  
Ruben Dario Motrich ◽  
Maria Laura Breser ◽  
Hugo Cejas ◽  
Cecilia Cuffini ◽  
...  
Keyword(s):  
Tract Infection ◽  
Genital Tract ◽  
Prostate Gland ◽  
Genital Tract Infection ◽  
Immune Reactions ◽  
Chlamydia Muridarum

scholarly journals Dissemination of Chlamydia trachomatis chronic genital tract infection in gamma interferon gene knockout mice.

1997 ◽  
Vol 65 (6) ◽  
pp. 2145-2152 ◽  
Author(s):  
T W Cotter ◽  
K H Ramsey ◽  
G S Miranpuri ◽  
C E Poulsen ◽  
G I Byrne
Keyword(s):  
Chlamydia Trachomatis ◽  
Tract Infection ◽  
Knockout Mice ◽  
Genital Tract ◽  
Gene Knockout ◽  
Gamma Interferon ◽  
Genital Tract Infection ◽  
Gene Knockout Mice ◽  
Interferon Gene

scholarly journals Chlamydia muridarumGenital and Gastrointestinal Infection Tropism Is Mediated by Distinct Chromosomal Factors

2018 ◽  
Vol 86 (7) ◽  
pp. e00141-18 ◽  
Author(s):  
Sandra G. Morrison ◽  
Amanda M. Giebel ◽  
Evelyn C. Toh ◽  
Horace J. Spencer ◽  
David E. Nelson ◽  
...  
Keyword(s):  
Tract Infection ◽  
Nonsense Mutation ◽  
Genital Tract ◽  
Genital Tract Infection ◽  
Nonsense Mutations ◽  
Content Type ◽  
Infectious Dose ◽  
Chlamydia Muridarum ◽  
Infection Models ◽  
Chromosomal Mutations

ABSTRACTSome members of the genusChlamydia, including the human pathogenChlamydia trachomatis, infect multiple tissues, including the genital and gastrointestinal (GI) tracts. However, it is unknown if bacterial targeting to these sites is mediated by multifunctional or distinct chlamydial factors. We previously showed that disruption of individual large clostridial toxin homologs encoded within theChlamydia muridarumplasticity zone were not critical for murine genital tract infection. Here, we assessed whether cytotoxin genes contribute toC. muridarumGI tropism. Infectivity and shedding of wild-type (WT)C. muridarumand three mutants containing nonsense mutations in different cytotoxin genes,tc0437,tc0438, andtc0439, were compared in mouse genital and GI infection models. One mutant, which had a nonsense mutation intc0439, was highly attenuated for GI infection and had a GI 50% infectious dose (ID50) that was 1,000 times greater than that of the WT. GI inoculation with this mutant failed to elicit anti-chlamydial antibodies or to protect against subsequent genital tract infection. Genome sequencing of thetc0439mutant revealed additional chromosomal mutations, and phenotyping of additional mutants suggested that the GI attenuation might be linked to a nonsense mutation intc0600. The molecular mechanism underlying this dramatic difference in tissue-tropic virulence is not fully understood. However, isolation of these mutants demonstrates that distinct chlamydial chromosomal factors mediate chlamydial tissue tropism and provides a basis for vaccine initiatives to isolate chlamydia strains that are attenuated for genital infection but retain the ability to colonize the GI tract and elicit protective immune responses.

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