ArticlePathogens and disease2015
Progesterone antagonizes the positive influence of estrogen on Chlamydia trachomatis serovar E in an Ishikawa/SHT-290 co-culture model.
Article in Pathogens and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Estrogen and bacterial infection.Frontiers in immunology · 2025Review
- Contributions of diverse models of the female reproductive tract to the study of Chlamydia trachomatis-host interactions.Current opinion in microbiology · 2024Review
- Progesterone and Inflammatory Response in the Oviduct during Physiological and Pathological Conditions.Cells · 2022Review
- Effect of Female Sex Hormones on the Immune Response againstPathogens (Basel, Switzerland) · 2022Article
- The hormonal environment and estrogen receptor signaling altersFrontiers in cellular and infection microbiology · 2022Article
- Effect of female sex hormones on the developmental cycle of Chlamydia abortus compared to a penicillin-induced model of persistent infection.BMC veterinary research · 2019Article
- The complexity of interactions between female sex hormones andCurrent clinical microbiology reports · 2019Article
- Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release.Scientific reports · 2017Article
- Inhibition of Wnt Signaling Pathways ImpairsFrontiers in cellular and infection microbiology · 2017Article
- Review
- Chlamydia cell biology and pathogenesis.Nature reviews. Microbiology · 2016Review
- Increased Risk of Endometriosis in Patients With Lower Genital Tract Infection: A Nationwide Cohort Study.Medicine · 2016Observational
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Studies indicate that estrogen enhances Chlamydia trachomatis serovar E infection in genital epithelial cells. Hormones have direct and indirect effects on endometrial epithelial cells. Estrogen and progesterone exposure induces endometrial stromal cells to release effectors that subsequently regulate growth and maturation of uterine epithelial cells. Estrogen enhances C. trachomatis infection by aiding entry and intracellular development in endometrial epithelial cell (Ishikawa, IK)/SHT-290 stromal cell co-culture. Enhanced chlamydial infection was mediated by direct estrogen-stimulated signaling events in epithelial cells and indirectly via estrogen-induced stromal cell effectors. The current study investigates the effects of hormones on chlamydial development using culture conditions representative of the menstrual cycle. Chlamydia trachomatis-infected IK or IK/SHT-290 cultures were exposed to 10(-8) M estrogen (E2), 10(-7) M progesterone (P4) or a combination of both hormones (10(-8) M E2 followed by 10(-9) M E2/10(-7) M P4). Chlamydial infectivity and progeny production were significantly decreased (30-66%) in cultures exposed to progesterone or estrogen/progesterone combination compared to estrogen alone. Thus, progesterone antagonized the positive effects of estrogen on chlamydial infection. These data indicate the susceptibility of endometrial epithelial cells to C. trachomatis infection during the menstrual cycle is altered by phase specific actions of sex hormones in the genital tract.
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Registered trials
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