ArticleInternational journal of medical sciences2007
Chlamydia trachomatis infection of human trophoblast alters estrogen and progesterone biosynthesis: an insight into role of infection in pregnancy sequelae.
Article in International journal of medical sciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Current Evidence of Maternal Infection With Chlamydia trachomatis and Preeclampsia Risk.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
- Estrogen and bacterial infection.Frontiers in immunology · 2025Review
- Host Lipid Manipulation by Intracellular Bacteria: Moonlighting for Immune Evasion.The Journal of membrane biology · 2023Review
- The mediating role of inflammation in the association between pregnancy loss history and gestational diabetes mellitus.Diabetology & metabolic syndrome · 2023Article
- Association of functional superoxide gene polymorphism with chlamydia trachomatis-associated recurrent spontaneous abortion.Molecular biology reports · 2023Article
- Chlamydia trachomatis antigen induces TLR4-TAB1-mediated inflammation, but not cell death, in maternal decidua cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Presence ofThe journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2021Article
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
- Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis.Mucosal immunology · 2013Article
- Association between history of abortion and metabolic syndrome in middle-aged and elderly Chinese women.Frontiers of medicine · 2013Article
- Modulation of cytokines and transcription factors (T-Bet and GATA3) in CD4 enriched cervical cells of Chlamydia trachomatis infected fertile and infertile women upon stimulation with chlamydial inclusion membrane proteins B and C.Reproductive biology and endocrinology : RB&E · 2009Article
- Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The trophoblast cells are in direct contact with endometrial tissues throughout gestation, playing important early roles in implantation and placentation. The physiologic significance and the operating mechanisms involved in probable altered trophoblast functions following Chlamydia trachomatis infection were investigated to determine if C. trachomatis initiates productive infection in trophoblast, effects of such event on the biosynthesis of cholesterol and its derivatives estrogen and progesterone; and the regulator of the biosynthesis of these hormones, human chorionic gonadotropin. Chlamydia trachomatis exhibited productive infection in trophoblast typified by inclusion formation observed when chlamydia elementary bodies were harvested from trophoblast and titrated onto HEp-2 cells. Assessment of the status of C. trachomatis in trophoblast showed a relative increase in protein of HSP-60 compared with MOMP, features suggestive of chlamydial chronicity. There was a decrease in cellular cholesterol of chlamydia infected trophoblast and a down regulation of HMG-CoA reductase. The levels of estrogen and progesterone were decreased, while the expression of aromatase and adrenodoxin reductase was up regulated. Also, there was a decrease in human chorionic gonadotropin expression. The implications of these findings are that C. trachomatis infection of trophoblast may compromise cellular cholesterol biosynthesis, thus depleting the substrate pool for estrogen and progesterone synthesis. This defect may impair trophoblast functions of implantation and placentation, and consequently affect pregnancy sequelae.
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