Characterization of beta2-adrenergic receptor homozygous knockout stress mouse model during Chlamydia muridarum genital infection

Abstract

Abstract The relationship of stress in chlamydia genital disease pathogenesis and its influence on the host immune response remains unknown. Beta2-adrenergic receptor(β2-AR), the major receptor of the stress hormone, norepinephrine (NE), is known to impair the function of immune cells. This study was undertaken to determine whether cold-induced stress (CIS) results in differential weight loss, stress hormone level production, and gene expression of β-AR subtypes in the β2-AR knockout (KO) and wildtype (WT) C57BL/J6 mice. CIS was induced by immersing mice in cold water for 5 minutes daily for 21 days, as per previously established protocols in our lab. CIS in 21 days resulted in average body or spleen weight loss of 1.88 or 0.018 gm, respectively, to β2-AR KO and 1.7 or 0.015 gm to WT C57BL/6J compared to their respective non-stressed group. Furthermore, β2-AR deficiency lead to a significant enhancement in C. muridarum shedding from days 9–15 following intravaginal infection, but no statistically significant difference between the stressed (4000 IFU/mL) and non-stressed (4200 IFU/ml) of β2-AR KO was obtained. β2-AR OK and WT stressed mice showed about 65–70 ng/mL production of NE; however, the intensity of C. muridarum infection was low in the KO than the WT (p <0.05). Relative fold-change in mRNA in splenic CD4+ T cells of stressed β2-AR OK was non-detectable. However, a slight upregulation of β1- and β3-AR was observed primarily in CD4+ T cells of β2-AR KO mice. Overall, the β2-AR and the WT C57BL/6J are related in many ways, and we predict to have similar physiological conditions suitable to compare pathogenies. Immunity, histopathology, and infertility.