Cold-induced stress modulates the maturation of immune cells of mice during Chlamydia muridarum genital infection

Abstract

Abstract Chlamydia genital infection caused by Chlamydia trachomatis is the most common bacterial sexually transmitted disease (STD) in the United States. Results in a cold-induced stress mouse model established in our laboratory show that cold-induced stress increases the intensity of chlamydia genital infection. This study was to survey the production of T helper cell type 1 (Th1) and (Th2) cytokines in the stress mouse model. Cells harvested from bone marrow or T cells from spleens of stressed and non-stressed mice during Chlamydia muridarum genital infection were allowed to proliferate in vitro. Cytokine production in culture supernatants was tested by ELISA. Gene expression of GATA 3, T-bet and INF-γ in splenic T cells were determined by QPCR. Production of IL-12 by dendritic cells of stressed mice was 0μg compared to 41.06 μg in non stressed mice. However, C. muridarum infection induced increased IL-12 production (97.27 μg and 123 μg) in stressed and non-stressed mice, respectively. Stress induced a 2-fold decrease in T-bet gene expression in T-cells compared to non-stressed group. In contrast, gene expression of GATA 3 in T cells of stressed mice was significantly increased compared to all other groups tested. INF-γ gene expression in T cells of stressed mice showed a 4-fold decrease compared to T cells of non stressed mice. Stress resulted in decreased IL-12 production in dendritic cells and macrophages, INF-γ production and gene expression of T-bet by Th1 cells. Furthermore, the increased gene expression of GATA 3 only in stressed chlamydia infected T cell suggests that cold-induced stress leads to a skewed immune response toward marked increase in production of Th2 cytokines that favor immunosuppression during chlamydia genital infection.