Roles of dendritic cells and macrophages during Chlamydia muridarum genital infection in stressed mice

It is well known that stress has a significant impact on public health and more evidence shows that stressors generally are greater in populations of lower socioeconomic status. Cold-induced stress inhibits immune cell activity and has been shown to cause different expressions of cytokine profiles during Chlamydia muridarum genital infection. Dendritic cells (DCs) and macrophages(MØ) are immune cells that express beta2-adrenergic receptor (β2-AR) and with key roles during chlamydia genital infection. This study is aimed to investigate the role of β2-AR by using a β2-AR knockout mouse. Wildtype (WT) and β2-AR knockout(KO) mice were stressed for five minutes daily and infected with C. muridarum intravaginally. Non-stressed infected mice of the groups were used as controls. Bone-marrow-derived DCs and MØ were tested isolated, counted differentiated, and proliferated for cytokine production. The proliferation of DCs and macrophages in the presence/absence of β2-AR agonists and antagonists was tested. Data show that non-stressed mice had a higher production of cytokines than stressed mice. Increased production of TNF-α in LPS-treated DCs and MØ of WT and β2-AR KO was observed. The effect of fenoterol and ICI118,55 antagonist showed no significant difference in cytokine production. The data indicate that β2-AR KO and WT had a similar pattern of cytokine production suggesting that deficiency in β2-AR restores the function of immune cells during genital infection. Experiments are undergoing to fully understand the mechanisms involved in modulating the function of DC and MØ during chlamydia genital infection.