scholarly journals LEVEL OF SEX HORMONES AND THE SEVERITY OF HYPERPLASTIC PROCESSES IN THE GENITAL TRACT IN WOMEN WITH CHRONIC CHLAMYDIAL INFECTION

2020 ◽  
Vol 1 (1) ◽  
pp. 23-31
Author(s):  
N. K. Guskova ◽  
E. V. Verenikina ◽  
T. Yu. Myagkova ◽  
A. P. Menshenina ◽  
E. A. Guskova ◽  
...  

Purpose of the study. To evaluate the role of chronic chlamydial infection in the genesis of proliferative processes in the female genital area.Materials and methods. The study involved 267 women aged from 27 to 43 years. Depending on the severity of the pathological process in the genital tract and the presence of the Chlamydia trachomatis infection, 6 groups were distinguished: 1st — 30 somatically healthy women without pathologies of the female reproductive system; 2nd and 3rd — those with inflammatory processes in the reproductive organs of non-chlamydial (36) and chlamydial nature (38); 4th and 5th — those with proliferative processes in the pelvic organs of non-chlamydial (50) and chlamydial nature (58); 6th — patients with cervical cancer (55). The PCR and ELISA (Chem Well, USA) methods were used to identify the presence of Chlamydia trachomatis. The concentration of estradiol (E) and progesterone (P) (ELISA) in the blood, as well as their ratio (E/P), was determined. The as-obtained data were compared with the results of cytomorphological and ultrasound studies.Results. Proliferative processes in the genital tract are accompanied by a change in the level of female sex hormones, in particular, by a sharp decrease in progesterone in the luteal phase of the cycle against the background of absolute or relative hyperestrogenism. These changes are more pronounced in women with chronic chlamydial infection. A connection between the presence of the infectious agent in question and the severity of hyperplastic processes in the female genital tract is established. A comparison of the obtained morphological data with the blood progesterone content in women without Chlamydia trachomatis showed that an increase in the severity of disorders correlates with a decrease in the level of female hormones. In women infected with Chlamydia trachomatis, the severity of hyperplastic processes shifts to the right, i. e. towards normal progesterone values. Therefore, even at maximal progesterone concentrations close to the reference values, a greater severity of pathological changes is observed.Conclusion. The obtained results demonstrate the undeniable role of chronic chlamydial infection in initiating a hormonal imbalance towards absolute or relative hyperestrogenia with a severe progesterone deficiency. A causal relationship of the Chlamydia trachomatis infectious agent with the severity of hyperplastic processes in the pelvic organs is established. It is concluded that the detection of chlamydial infection should be considered as an essential element in the screening and prevention of hyperplastic processes.

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.


2022 ◽  
Author(s):  
Xin Su ◽  
Hong Xu ◽  
Maegan French ◽  
Yujie Zhao ◽  
Lingli Tang ◽  
...  

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.


2007 ◽  
Vol 76 (2) ◽  
pp. 515-522 ◽  
Author(s):  
Wen Cheng ◽  
Pooja Shivshankar ◽  
Zhongyu Li ◽  
Lili Chen ◽  
I-Tien Yeh ◽  
...  

ABSTRACT Chlamydia trachomatis infection induces inflammatory pathologies in the upper genital tract, potentially leading to ectopic pregnancy and infertility in the affected women. Caspase-1 is required for processing and release of the inflammatory cytokines interleukin-1β (IL-1β), IL-18, and possibly IL-33. In the present study, we evaluated the role of caspase-1 in chlamydial infection and pathogenesis. Although chlamydial infection induced caspase-1 activation and processing of IL-1β, mice competent and mice deficient in caspase-1 experienced similar courses of chlamydial infection in their urogenital tracts, suggesting that Chlamydia-activated caspase-1 did not play a significant role in resolution of chlamydial infection. However, when genital tract tissue pathologies were examined, the caspase-1-deficient mice displayed much reduced inflammatory damage. The reduction in inflammation was most obvious in the fallopian tube tissue. These observations demonstrated that although caspase-1 is not required for controlling chlamydial infection, caspase-1-mediated responses can exacerbate the Chlamydia-induced inflammatory pathologies in the upper genital tract, suggesting that the host caspase-1 may be targeted for selectively attenuating chlamydial pathogenicity without affecting the host defense against chlamydial infection.


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

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