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

• Published in: Pathogens and disease 2024-02, Vol.82
• Main Authors: Belay, Tesfaye, Sahu, Rajnish, Dennis, Vida, Cook, Kaitlyn, Ray, Alexis, Baker, Danielle, Kelly, Ashlei, Woart, Nathasha
• Format: Article
• Language: English
• Subjects: Animals; CD4-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - immunology; Chlamydia Infections - immunology; Chlamydia Infections - microbiology; Chlamydia muridarum - immunology; Cytokines - metabolism; Disease Models, Animal; Female; Interferon-gamma - metabolism; Mice; Mice, Knockout; Norepinephrine - metabolism; Receptors, Adrenergic, beta-2 - deficiency; Receptors, Adrenergic, beta-2 - genetics; Receptors, Adrenergic, beta-2 - metabolism; Reproductive Tract Infections - immunology; Reproductive Tract Infections - microbiology
• ISSN: 2049-632X; 2049-632X
• DOI: 10.1093/femspd/ftae029

Chlamydia genital infection caused by Chlamydia trachomatis is the most common bacterial sexually transmitted disease worldwide. A mouse model has been developed in our laboratory to better understand the effect of cold-induced stress on chlamydia genital infection and immune response. However, the stress mechanism affecting the host response to Chlamydia muridarum genital infection remains unclear. Here, we demonstrate a role for the beta2-adrenergic receptor (β2-AR), which binds noradrenaline and modulates the immune response against chlamydia genital infection in a mouse model. A successful β2-AR homozygous knockout (KO) mouse model was used to study the infection and analyze the immune response. Our data show that stressed mice lacking the β2-AR are less susceptible to C. muridarum genital infection than controls. A correlation was obtained between lower organ load and higher interferon-gamma production by CD4+ and CD8+ cells of the KO mice. Furthermore, exposure of CD4+ T cells to noradrenaline alters the production of cytokines in mice during C. muridarum genital infection. This study suggests that the blockade of β2-AR signaling could be used to increase resistance to chlamydia genital infection. We value the β2-AR KO as a viable model that can provide reproducible results in investigating medical research, including chlamydia genital infection.