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Pre-Treatment with Estradiol, But not Progesterone, Exacerbates DSS Colitis: Dysregulated Innate Immunity and
Anja Hjelt1, Lauri Polari2,3,4, Heli Jokela2,5,4
1Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, Turku, 20520, Finland. hjeltanja@gmail.com.
Inflammation
|July 2, 2026
Summary
Estradiol exacerbates intestinal inflammation in female mice, contrary to some prior studies. This research highlights estradiol
Area of Science:
- Gastroenterology
- Immunology
- Endocrinology
Background:
- Epidemiological studies suggest a link between inflammatory bowel disease (IBD) and female sex hormones.
- Previous preclinical research on estradiol's role in colitis yielded conflicting results.
Purpose of the Study:
- To investigate the effects of estradiol and progesterone on dextran sulfate sodium (DSS)-induced colitis in female mice.
- To explore the role of estrogen receptors in mediating colonic inflammation.
Main Methods:
- Utilized ovariectomized and sham-operated female mice, with and without hormonal supplementation (estradiol and progesterone).
- Induced colitis using dextran sulfate sodium (DSS).
- Analyzed inflammatory markers and gene expression profiles.
Main Results:
- Estradiol supplementation, with or without progesterone, significantly worsened intestinal inflammation in mice.
- Progesterone alone did not alter the inflammatory status.
- Estradiol exposure altered gene expression related to antimicrobial response, immune cell activation, and epithelial integrity.
Conclusions:
- Provides strong evidence that estradiol acts as an inflammatory agent in the colon of female mice, particularly with longer-term exposure.
- Suggests a potential mechanism involving estrogen receptor signaling in exacerbating colitis.
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