Determining the role of Regulatory T Cells in a β2-Adrenergic Receptor Knockout Mouse Model during Chlamydia muridarum Infection.

Abstract

Regulatory T cells (Tregs) are a form of white blood cells that regulate immune response when encountered with pathogens. Previous studies have shown that Tregs play a critical role in promoting the function of Thelper 17 and suppressing the function of Thelper 1 cells during chlamydia genital infection in mice. However, studies have not yet been conducted on the role of Tregs in our stress mouse model during Chlamydia muridarum (Cm) genital infection. We hypothesized that cold-induced stress affects the profiles of transcription factor and signature cytokine production of regulatory T cells during Cm genital infection. The objective of the study was to determine the gene expression of the transcription factor of FoxP3 and key cytokines of the stressed and non-stressed beta2-adregenic receptor (b2-AR) knockout (KO) mouse during Cm. The experimental group stressed or non-stressed β2-AR KO or C57BL/6J wildtype (WT) mice. Stress was induced by placing the mice in 4° C water for 5 minutes daily for 21 days, and the mice were infected intravaginally with Cm. The 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 FoxP3 and interleukin-10 production 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.