Profile of CD8+ T-cells in a Stressed beta2- Adrenergic Receptor Knockout Mouse Model during Chlamydia muridarum Genital Infection.

Abstract

Chlamydia trachomatis is the most common bacterial sexually transmitted disease. A negative correlation between the immune system and stress has been reported. We have demonstrated that cold-induced stress (CIS) increases the intensity of Chlamydia muridarum genital infection in a mouse model, but the status of CD8+ T cells is still unknown. This study profiles CD8+ T cell’s interaction with stress hormone; norepinephrine (NE) and the beta2-adrenergic receptor (β2-AR) in the presence of agonists and antagonists; and examines cytokines produced in the β2-AR knockout (KO) stress mouse model during C. muridarum genital infection.   We hypothesize that CD8+ T cells produce high-level IFN-g and low-level TNF-a in stressed β2-AR KO mice than C57BL/6J wildtype (WT).   Two groups of mice were cold-water stressed for 21 days, infected with C. muridarum, and then sacrificed for CD8+ T cell isolation. Viability was tested. The proliferation of CD8+ T cells was carried out for 72 h and culture supernatant was collected for cytokine production using ELISA. To confirm genital tract infection, Chlamydia muridarum isolation is underway. Our data show that the viability of CD8+ T cells treated with NE was significantly reduced compared to cells treated with LPS or Con A, indicating the suppressive effect of NE on immune cells. Stressed β2-AR KO mice displayed increased production of protective cytokines compared to stressed WT mice, indicating the absence of β2-AR leads to the functional restoration of protective immune cells.