Chlamydia is the most commonly reported sexually transmitted infection in the US, with an estimated 4 million new cases in 2018 alone. In addition to humans, Chlamydia infects other animals including mice, and mice have become a popular model for the study of Chlamydia infection. Female sex hormones (FSH) estrogen (E2) and progesterone (P4) rise and fall in a cyclic fashion in both humans and mice, and it is well established that these hormones affect the establishment and progression of genital chlamydial infection. Prior studies that used a co-culture model of human endometrial epithelial cells (IK cells) grown on extracellular matrix-coated inserts over human stromal cells (SHT cells) showed that E2 treatment enhanced initial chlamydial infection and production of progeny Chlamydia compared to hormone free (HF), P4 or combination E2’E2/P4 treatment. This led to the hypothesis that the treatment of ovariectomized (OVX) mice with E2 would enhance chlamydial infection compared to mice treated with no hormone, P4, or a combination of E2 and P4. We ordered OVX mice from Jackson Laboratories and surgically implanted silastic capsules that contained E2, P4, E2/P4, or no hormone diluted in sesame oil. A gas chromatography method was developed to test E2 and P4 concentration in mouse serum, ensuring that hormone levels were physiologically relevant. 8 days after the implantation of the capsules, mice were vaginally-inoculated with C. muridarum¸ a chlamydial species that mimics human chlamydial infection in mice. Every 3 days post infection (pi), for 21 days, we vaginally swabbed mice to determine how much C. muridarum each mouse shed and created a graphical representation of chlamydial shedding. A subset of mice were sacrificed on day 10pi so that presence and identity of immune cells could be analyzed by flow cytometry. Surprisingly, E2 alone and E2/P4 treatment completely protected mice from chlamydial infection. HF-treated mice peaked in chlamydial shedding on day 3pi, and P4-treated mice peaked on day 9pi. Flow cytometry data showed that E2-treated mice had a significantly reduced T cell presence in the genital tract. Thus far, our data suggest that FSH affect chlamydial infection in mice differently than in humans. This observation could have important implications for a field that is heavily reliant on murine studies.
| Identifer | oai:union.ndltd.org:ETSU/oai:dc.etsu.edu:asrf-1771 |
| Date | 18 March 2021 |
| Creators | Gravitte, Amy, Kintner, Jen, Brown, Stacy, Kennard, Benjamin, Cobble, Allison, Hall, Jennifer |
| Publisher | Digital Commons @ East Tennessee State University |
| Source Sets | East Tennessee State University |
| Detected Language | English |
| Type | text |
| Source | Appalachian Student Research Forum |
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