THE EFFECTS OF ESTROGEN-INDUCED STROMAL CELL EFFECTORS, OSTEOPONTIN AND VIMENTIN, ON CHLAMYDIA INFECTIONS IN A NON-POLARIZED CELL CULTURE MODEL
Location
RIPSHIN MTN. ROOM 130
Start Date
4-4-2018 10:00 AM
End Date
4-4-2018 10:15 AM
Name of Project's Faculty Sponsor
Dr. Jennifer Hall
Faculty Sponsor's Department
Department of Biomedical Sciences and the Center for Infectious Disease, Inflammation and Immunity, Quillen College of Medicine
Type
Oral Presentation
Project's Category
Biomedical and Health Sciences
Abstract or Artist's Statement
Chlamydia is the most reported sexually transmitted infection in the US and is caused by the obligate intracellular bacterium Chlamydia trachomatis. Typically, this presents as a lower genital tract infection (cervicitis or urethritis), but can ascend to the upper genital tract, causing pelvic inflammatory disease, tubal infertility, epididymitis, or ectopic pregnancy. While chlamydia infections can be cured with a single-dose oral antibiotic, repeat infections are common and having multiple chlamydial infections increases a woman’s risk of developing serious chronic conditions. Previous research has shown that estrogen has a positive effect on C. trachomatis infections—an important finding, connecting fluctuating estrogen levels in females to variance in pathogenesis.The mechanism behind this hormonal influence remains unknown; however, previous work in our laboratory indicates that estrogen-stimulated stromal cell effectors play a role in enhancing C. trachomatis infections in a polarized endometrial epithelial Ishikawa (IK)/stromal (SHT-290) cell co-culture model. Specifically, our data indicate that estrogen exposure stimulates osteopontin and vimentin release from stromal cells in co-culture with endometrial epithelial cells. Furthermore, we noted that Chlamydia-infected, polarized Ishikawa cells exposed to a combination of recombinant osteopontin and estrogen released significantly more infectious chlamydia than cultures exposed to estrogen alone. Most tissue culture models being used today employee non-polarized cells. Given the fact that epithelial cell polarization is known to impact C. trachomatis serovar E development, in the current study we sought to determine if the estrogen-induced stromal cell effectors, osteopontin and vimentin, affect C. trachomatis viability and infectivity in non-polarized Ishikawa cells. Non-polarized Ishikawa cells were exposed to osteopontin or vimentin in the presence or absence of estrogen, infected with C. trachomatis serovar E, and collected for examination of chlamydial infectivity and progeny production. Our initial data show that osteopontin and vimentin impact chlamydial progeny production in a concentration dependent fashion, with higher concentrations of recombinant effectors +/- estrogen significantly decreasing progeny production. These data suggest that polarization of host cells influences the way hormone-stimulated effectors interact with the cell to impact on chlamydial infection. Future research goals are to explore other stromal effectors such as fibronectin with estrogen and to study the cell signaling mechanism osteopontin and vimentin use to affect chlamydial infections in polarized epithelial cell cultures.
THE EFFECTS OF ESTROGEN-INDUCED STROMAL CELL EFFECTORS, OSTEOPONTIN AND VIMENTIN, ON CHLAMYDIA INFECTIONS IN A NON-POLARIZED CELL CULTURE MODEL
RIPSHIN MTN. ROOM 130
Chlamydia is the most reported sexually transmitted infection in the US and is caused by the obligate intracellular bacterium Chlamydia trachomatis. Typically, this presents as a lower genital tract infection (cervicitis or urethritis), but can ascend to the upper genital tract, causing pelvic inflammatory disease, tubal infertility, epididymitis, or ectopic pregnancy. While chlamydia infections can be cured with a single-dose oral antibiotic, repeat infections are common and having multiple chlamydial infections increases a woman’s risk of developing serious chronic conditions. Previous research has shown that estrogen has a positive effect on C. trachomatis infections—an important finding, connecting fluctuating estrogen levels in females to variance in pathogenesis.The mechanism behind this hormonal influence remains unknown; however, previous work in our laboratory indicates that estrogen-stimulated stromal cell effectors play a role in enhancing C. trachomatis infections in a polarized endometrial epithelial Ishikawa (IK)/stromal (SHT-290) cell co-culture model. Specifically, our data indicate that estrogen exposure stimulates osteopontin and vimentin release from stromal cells in co-culture with endometrial epithelial cells. Furthermore, we noted that Chlamydia-infected, polarized Ishikawa cells exposed to a combination of recombinant osteopontin and estrogen released significantly more infectious chlamydia than cultures exposed to estrogen alone. Most tissue culture models being used today employee non-polarized cells. Given the fact that epithelial cell polarization is known to impact C. trachomatis serovar E development, in the current study we sought to determine if the estrogen-induced stromal cell effectors, osteopontin and vimentin, affect C. trachomatis viability and infectivity in non-polarized Ishikawa cells. Non-polarized Ishikawa cells were exposed to osteopontin or vimentin in the presence or absence of estrogen, infected with C. trachomatis serovar E, and collected for examination of chlamydial infectivity and progeny production. Our initial data show that osteopontin and vimentin impact chlamydial progeny production in a concentration dependent fashion, with higher concentrations of recombinant effectors +/- estrogen significantly decreasing progeny production. These data suggest that polarization of host cells influences the way hormone-stimulated effectors interact with the cell to impact on chlamydial infection. Future research goals are to explore other stromal effectors such as fibronectin with estrogen and to study the cell signaling mechanism osteopontin and vimentin use to affect chlamydial infections in polarized epithelial cell cultures.