SUMMARY
Recent studies have shown that Chlamydia muridarum causes a lung infection that resembles pneumonia of C. trachomatis in humans. However, the mechanism(s) of the infection is/are not well defined. Dendritic cells (DCs) play a significant role in protection against Chlamydia genital infections, but their role during stressful conditions is unknown. This study is to examine the role of bone marrow-derived dendritic cells (BMDCs) in beta2-adrenergic receptor (ß2-AR) knockout (KO) male mice during C. muridarum lung infection. We hypothesized that the lack of ß2-AR leads to decreased organ load of C. muridarum in mice lung infection. We also hypothesized that BMDCS from ß2-AR KO mice restored the normal function of cytokine production and served as an antigen-presenting activity to CD4+T cells. Stressed and non-stressed C57BL/6J wildtype (WT) and ß2-AR gene knockout mice will be infected. Lysates of lungs will be tested for isolation of C. muridarum. Cells will be for Differentiation and proliferation of BMDCs will be performed to detect cytokine production. Results should correspond to our working hypothesis, which includes the lack of (ß2-AR) leads to decreased organ load of C. muridarum in lung infection. Results will show significant differences between stressed ?2-AR KO and stressed of WT. Moreover, increased protective cytokine production in stressed ?2-AR KO compared to decreased cytokines production in stressed WT will be observed. Our findings may suggest that mice lacking b2 AR have reverted to protective cytokine production to reduce infection, and the function of BMDCs as antigen-presenting cells will be restored in KO mice.