CYTOLOGICAL DIAGNOSIS OF CHLAMYDIAL INFECTION OF FEMALE GENITAL TRACT

The Lancet ◽  
1983 ◽  
Vol 321 (8339) ◽  
pp. 1449 ◽  
Author(s):  
Gabriele Medley
The Lancet ◽  
1983 ◽  
Vol 322 (8349) ◽  
pp. 578-579
Author(s):  
G Forster ◽  
R Jha ◽  
D Cheetham ◽  
P Munday ◽  
D Coleman ◽  
...  

2000 ◽  
Vol 68 (1) ◽  
pp. 192-196 ◽  
Author(s):  
Hua Su ◽  
Ronald Messer ◽  
William Whitmire ◽  
Scott Hughes ◽  
Harlan D. Caldwell

ABSTRACT Chlamydia trachomatis is a major cause of sexually transmitted disease (STD) for which a vaccine is needed. CD4+ T-helper type 1 (Th1) cell-mediated immunity is an important component of protective immunity against murine chlamydial genital infection. Conventional vaccine approaches have not proven effective in eliciting chlamydial-specific CD4 Th1 immunity at the genital mucosa. Thus, it is possible that the development of a highly efficacious vaccine against genital infection will depend on the generation of a live attenuated C. trachomatis vaccine. Attenuated strains of C. trachomatis do not exist, so their potential utility as vaccines cannot be tested in animal models of infection. We have developed a surrogate model to study the effect of chlamydial attenuation on infection and immunity of the female genital tract by treating mice with a subchlamydiacidal concentration of oxytetracycline following vaginal infection. Compared to untreated control mice, antibiotic-treated mice shed significantly fewer infectious organisms (3 log10) from the cervico-vagina, produced a minimal inflammatory response in urogenital tissue, and did not experience infection-related sequelae. Antibiotic-treated mice generated levels of chlamydia-specific antibody and cell-mediated immunity equivalent to those of control mice. Importantly, antibiotic-treated mice were found to be as immune as control untreated mice when rechallenged vaginally. These findings demonstrate that subclinical chlamydial infection of the murine female genital tract is sufficient to stimulate a potent protective immune response. They also present indirect evidence supporting the possible use of live attenuated chlamydial organisms in the development of vaccines against chlamydial STDs.


1985 ◽  
Vol 12 (2) ◽  
pp. 68-71 ◽  
Author(s):  
ERIC M. C. DUNLOP ◽  
BENG T. GOH ◽  
SOHRAB DAROUGAR ◽  
RALPH WOODLAND

1999 ◽  
Vol 67 (10) ◽  
pp. 5518-5521 ◽  
Author(s):  
James I. Ito ◽  
Joseph M. Lyons

ABSTRACT Earlier investigations have not shown an important role for gamma interferon (IFN-γ) in the early clearance of chlamydial infection from the murine female genital tract. In a model using a human genital isolate of Chlamydia trachomatis in IFN-γ and IFN-γ receptor knockout mice, we were able to demonstrate a major role for IFN-γ in mediating control of infection throughout the course of infection.


2021 ◽  
Author(s):  
Svenja Barth ◽  
Susanne Kirschnek ◽  
Noemi Ortmann ◽  
Yakup Tanriver ◽  
Georg Häcker

Background Innate lymphoid cells (ILCs) are comprised of five distinct subsets. ILCs are found at mucosal barriers and may fight invading pathogens. Chlamydia is an intracellular bacterium that infects the mucosa of the genital tract and can cause severe tissue damage. Methods We used a mouse infection model with Chlamydia muridarum ( Cmu ) to measure the reaction of genital tract ILCs to the infection. Results Tissue resident natural killer cells were the largest group in the uninfected female genital tract, and their number did not substantially change. Conventional NK cells were present at the greatest numbers during acute infection, while ILC1 cells continuously increased to high numbers. ILC2 and ILC3 cells were found at lower numbers that oscillated by a factor of 2-4. The majority of ILC3 transdifferentiated into ILC1 cells. NK cells and ILC1 cells produced IFN-γ and, rarely, TNF, but only early in the infection. Lack of B and T cells increased, while the loss of myeloid cells decreased ILC numbers. ILCs accumulated to high density in the oviduct, a main site of tissue destruction. Conclusions ILC subsets are part of the inflammatory and immune reaction during infection with Cmu and may contribute to tissue damage during chlamydial infection.


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