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Major Project

Immunopathogenesis of Chlamydia in a stress mouse model

Research in our laboratory focuses on understanding the mechanism (s) by which stress alters immune response which leads to increased intensity of genital infection mice. Data from our laboratory demonstrated 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 were detected. We 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 genital infection in humans.