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Polycystic ovary syndrome (PCOS) is linked to reproductive infections by atypical pathogens like Chlamydia trachomatis. These infections trigger an inflammatory immune response, potentially worsening PCOS complications and impacting fertility.

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Area of Science:

  • Reproductive Endocrinology
  • Microbiology
  • Immunology

Background:

  • Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women, associated with hormonal imbalances, metabolic issues, and fertility challenges.
  • PCOS is increasingly linked to alterations in the vaginal microbiome, inflammation, and susceptibility to pathogenic microorganisms.
  • Atypical pathogens, including Chlamydia trachomatis, Mycoplasma hominis, and Ureaplasma spp., are implicated in reproductive system infections.

Purpose of the Study:

  • To investigate the prevalence of atypical pathogen infections (Chlamydia trachomatis, Mycoplasma hominis, Ureaplasma spp.) in women with PCOS.
  • To assess the immune system's response by measuring serum proinflammatory cytokines (IL-1β, IL-6, TNF-α) in relation to these infections.
  • To explore the correlation between atypical pathogen infections, cytokine levels, and PCOS-related complications.

Main Methods:

  • Analysis of reproductive system infections in 490 women with PCOS (aged 26-43) for C. trachomatis, M. hominis, and Ureaplasma spp.
  • Measurement of serum IL-1β, IL-6, and TNF-α levels in infected PCOS patients (n=196) and comparison with PCOS controls (n=39) and healthy controls (n=28).
  • Evaluation of clinical features and vaginal biocenosis findings, alongside targeted testing for atypical pathogens.

Main Results:

  • A 40% infection rate with atypical pathogens was found in the PCOS group, with C. trachomatis (17.7%) being most prevalent, followed by Ureaplasma spp. (10%) and M. hominis (4.9%).
  • Co-infections were observed in 3.1% (Mycoplasma/Ureaplasma) and 4.3% (all three pathogens).
  • Elevated levels of IL-1β, IL-6, and TNF-α were noted in infected PCOS patients, particularly with C. trachomatis, suggesting a significant immune response.

Conclusions:

  • Infections with atypical pathogens like C. trachomatis and genital mycoplasmas can disrupt reproductive health and contribute to infertility in women with PCOS.
  • The observed immune response, characterized by increased proinflammatory cytokines (TNF-α, IL-1β, IL-6), may exacerbate inflammation and tissue damage.
  • Extended diagnostics for atypical pathogens are crucial for PCOS management, given their association with heightened immune responses and potential complications.