UC Merced

Chlamydia trachomatis is the most common bacterial sexually transmitted infection amongst individuals between the ages of 14-39 within the United States [1]. The immune system responds to the recognition of Chlamydia infection by inducing an inflammatory response and recruiting T cells to fight the pathogen. The proposed experiment evaluates whether pregnancy has an influence on the course of Chlamydia muridarum infection in a murine model. Previous studies show production of type 1 helper T cells (T_h1) are important for aiding in the clearance of Chlamydia. However, pregnancy elicits type 2 helper T cells (T_h2) to protect the fetus, which aren't effective in fighting an infection.[2] In my experiment, pregnant and nonpregnant C57BL/6 mice were infected with Chlamydia muridarum. Vaginal secretion and vaginal swabs were collected everyday for eleven days. It is hypothesized a T_h2 cytokine production will not protect against Chlamydia infection, but may contribute to the development of persistent infection. In my study, infection can be tracked without sacrificing mice at different time points. This allows for minimal usage of mice. It will also illustrate a real-time course of infection throughout pregnancy. The findings provide a murine model that can be applied in illustrating the possible outcomes of infection in humans during pregnancy.