Examining the role of T helper17 cells in a beta-2 adrenergic receptor knockout stress mouse model during Chlamydia muridarum genital infection.

Abstract

Chlamydia trachomatis is the most common bacterial sexually transmitted disease in the world. The correlation between stress in chlamydia genital pathogenesis and its effects on host immune response is not well-studied. Norepinephrine (NE), a stress hormone, binds and activates the beta-2 (AR), which is expressed by CD4+(T-cells) of the spleen and lymph nodes. Regulatory T cells are known to promote Th17 responses and genital tract inflammation upon intracellular Cm infection, but the mechanisms during stress are not known. A cold-water-induced mouse model is used to induce stress and explore the relationship between stress and Chlamydia muridarum (Cm) genital infection. We hypothesize that T-helper 17 cells and Tumor Necrosis Factor-alpha (TNF-a) play an important role in the production and development of immunopathology in stressed mice. Wildtype and beta-2 adrenergic receptor (b2-AR) knockout (KO) mice were stressed for five minutes every day for 21 days subsequently infected with Cm intravaginally. Total T cells were harvested from the spleen and lymph nodes and purified using Stem Cell Technologies kits and proliferated for 32 or 72 hours for RNA isolation and qPCR analysis or cytokine detection using ELISA, respectively. Currently, data collection and analysis are underway. We expect decreased gene expression of and interleukin-17 production in b2-AR KO, indicating the downregulation of Treg cells in stressed mice. The obtained data may provide insights into preventing and controlling Cm genital infection during stressful conditions.