Progesterone antagonizes the positive influence of estrogen on Chlamydia trachomatis serovar E in an Ishikawa/SHT-290 co-culture model.
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.
Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0579, USA.
Jennifer
J
Kintner
Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0579, USA Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Robert V
RV
Schoborg
Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0579, USA.
Priscilla B
PB
Wyrick
Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0579, USA Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA halljl1@etsu.edu.
Jennifer V
JV
Hall
D002460:Cell Line; D002692:Chlamydia trachomatis / Q000145:classification / Q000187:drug effects* / Q000254:growth & development*; D018920:Coculture Techniques; D004705:Endocytosis; D004847:Epithelial Cells / Q000187:drug effects* / Q000382:microbiology*; D004967:Estrogens / Q000378:metabolism*; D005260:Female; D006801:Humans; D011374:Progesterone / Q000378:metabolism*; D065288:Serogroup
D004967:Estrogens; D011374:Progesterone
Chlamydia trachomatis; endometrial stromal cells; epithelial/stromal cell co-culture; estrogen; polarized endometrial cells; progesterone