CHLAMYDIA TRACHOMATIS IN THE UPPER FEMALE GENITAL TRACT WITH NEGATIVE CERVICAL CULTURE

The Lancet ◽  
1986 ◽  
Vol 328 (8503) ◽  
pp. 390 ◽  
Author(s):  
BirgerR. Møller ◽  
Pia Kaspersen ◽  
FrankV. Kristiansen ◽  
Per-Anders Mårdh
Keyword(s):  
Chlamydia Trachomatis ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Female Genital

Evidence for cGAS-STING signaling in the female genital tract resistance to Chlamydia trachomatis infection

2022 ◽  
Author(s):  
Xin Su ◽  
Hong Xu ◽  
Maegan French ◽  
Yujie Zhao ◽  
Lingli Tang ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Chlamydia Trachomatis ◽  
Signaling Pathway ◽  
Genital Tract ◽  
Essential Role ◽  
Cultured Cells ◽  
Female Genital Tract ◽  
Lower Genital Tract ◽  
Female Genital

Sexually transmitted Chlamydia trachomatis can ascend to the upper genital tract due to its resistance to innate immunity in the lower genital tract. C. trachomatis can activate cGAS-STING signaling pathway in cultured cells via either cGAS or STING. The current study was designed to evaluate the role of the cGAS-STING pathway in innate immunity against C. trachomatis in the mouse genital tract. Following intravaginal inoculation, C. trachomatis significantly declined by day 5 following a peak infection on day 3 while the mouse-adapted C. muridarum continued to rise for >1 week, indicating that C. trachomatis is susceptible to the innate immunity in the female mouse genital tract. This conclusion was supported by the observation of a similar shedding course in mice deficient in adaptive immunity. Thus, C. trachomatis can be used to evaluate innate immunity in the female genital tract. It was found that mice deficient in either cGAS or STING significantly increased the yields of live C. trachomatis on day 5, indicating an essential role of the cGAS-STING signaling pathway in innate immunity of the mouse genital tract. Comparison of live C. trachomatis recovered from different genital tissues revealed that the cGAS-STING-dependent immunity against C. trachomatis was restricted to the mouse lower genital tract regardless of whether C. trachomatis was inoculated intravaginally or transcervically. Thus, we have demonstrated an essential role of the cGAS-STING signaling pathway in innate immunity against chlamydial infection, laying a foundation for further illuminating the mechanisms of the innate immunity in the female lower genital tract.

scholarly journals Animal Models for Studying Female Genital Tract Infection with Chlamydia trachomatis

2013 ◽  
Vol 81 (9) ◽  
pp. 3060-3067 ◽  
Author(s):  
Evelien De Clercq ◽  
Isabelle Kalmar ◽  
Daisy Vanrompay
Keyword(s):  
Chlamydia Trachomatis ◽  
Animal Models ◽  
Genital Tract ◽  
Transmitted Disease ◽  
Female Genital Tract ◽  
Genital Tract Infection ◽  
Content Type ◽  
Genital Tract Infections ◽  
Tract Infections ◽  
Female Genital

ABSTRACTChlamydia trachomatisis a Gram-negative obligate intracellular bacterial pathogen. It is the leading cause of bacterial sexually transmitted disease in the world, with more than 100 million new cases of genital tract infections withC. trachomatisoccurring each year. Animal models are indispensable for the study ofC. trachomatisinfections and the development and evaluation of candidate vaccines. In this paper, the most commonly used animal models to study female genital tract infections withC. trachomatiswill be reviewed, namely, the mouse, guinea pig, and nonhuman primate models. Additionally, we will focus on the more recently developed pig model.

scholarly journals Immune Pathogenesis of Asymptomatic Chlamydia trachomatis Infections in the Female Genital Tract

1995 ◽  
Vol 3 (4) ◽  
pp. 169-174 ◽  
Author(s):  
Steven S. Witkin
Keyword(s):  
Chlamydia Trachomatis ◽  
Genital Tract ◽  
Pregnancy Loss ◽  
Early Stage ◽  
Female Genital Tract ◽  
In Vivo Studies ◽  
Fallopian Tubes ◽  
Female Genital

Chlamydia trachomatis (CT) infections of the female genital tract, although frequently asymptomatic, are a major cause of fallopian-tube occlusion and infertility. Early stage pregnancy loss may also be due to an unsuspected and undetected CT infection. In vitro and in vivo studies have demonstrated that this organism can persist in the female genital tract in a form undetectable by culture. The mechanism of tubal damage as well as the rejection of an embryo may involve an initial immune sensitization to the CT 60 kD heat shock protein (HSP), followed by a reactivation of HSP-sensitized lymphocytes in response to the human HSP and the subsequent release of inflammatory cytokines. The periodic induction of human HSP expression by various microorganisms or by noninfectious mechanisms in the fallopian tubes of women sensitized to the CT HSP may eventually result in tubal scarring and occlusion. Similarly, an immune response to human HSP expression during the early stages of pregnancy may interfere with the immune regulatory mechanisms required for the maintenance of a semiallogeneic embryo.

scholarly journals Human Female Genital Tract Infection by the Obligate Intracellular Bacterium Chlamydia trachomatis Elicits Robust Type 2 Immunity

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e58565 ◽  
Author(s):  
Rodolfo D. Vicetti Miguel ◽  
Stephen A. K. Harvey ◽  
William A. LaFramboise ◽  
Seth D. Reighard ◽  
Dean B. Matthews ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Tract Infection ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Obligate Intracellular Bacterium ◽  
Human Female ◽  
Genital Tract Infection ◽  
Obligate Intracellular ◽  
Female Genital
Sign in / Sign up

Export Citation Format

Share Document