Immunopathogenesis of Chlamydia in a stress mouse model
Research in Dr. Belay’s laboratory focuses on understanding the mechanism (s) by which stress increases intensity of genital infection and alterations of immune response in a mouse model. Genital infection by Chlamydia trachomatis, the most common bacterial sexually transmitted disease worldwide, has long-term health complications such as pelvic inflammatory disease, ectopic pregnancy, and infertility in women. Biological, epidemiological and clinical studies of the chlamydia genital infection is well documented, however, the relationship of stress in the pathogenesis of Chlamydia trachomatis and its influence on the host immune response remains unknown. Chlamydia has high prevalence in populations of low socioeconomic status, but stress is speculated as one of risk factors to play a big role in enhancing infection. Dr. Belay’s data demonstrates that exposure of mice to cold-water stress results in elevated levels of norepinephrine or epinephrine in spleens and genital tract lysates. Moreover, decreased mRNA and protein level of cytokines and chemokines in genital tract lysates of stressed mice have been detected. Dr. Belay and students are currently characterizing the influence of cold-induced stress on i) distribution pattern of immune cells in the different regions of the genital tract; ii) histopathological changes; iii) chlamydia-induced infertility in the mouse model to elucidate the mechanism(s) by which stress hormones increase intensity of chlamydia genital infection in the stress model. Thus understanding the interaction between stress, immune system and infection is significant for the management of chlamydia infection.