PRJNA866545
The hormonal environment and estrogen receptor signaling alters Chlamydia muridarum infection in murine infection models via the immune response.
Genital Chlamydia is the most common bacterial sexually transmitted infection in the United States and worldwide. Previous studies indicate that chlamydial infections are influenced by various factors, including the female sex hormones estrogen and progesterone. Varying concentrations of estrogen and progesterone may impact the progression of chlamydial infection and the host's immune response to Chlamydia. Estrogen signals through estrogen receptors (ERs), ER alpha and ER beta. These receptors are similar in structure and function, but are differentially expressed in the tissues throughout the genital tract and immune system. Here we examined the effects of ER signaling on C. muridarum infection using ER alpha or ER beta knockout mouse strains. We found that the absence of ER alpha, but not ER beta significantly altered chlamydiae shedding. We used TruSeq targeted RNA sequencing to examine the effect of ERs on expression of immune markers during chlamydial infection. These data indicate that ER signaling alters the T cell response to chlamydial infection.