Research Interests:Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infection (STI) in the United States, with an estimated 3-5 million new cases per year, as well as the leading cause of preventable blindness worldwide. Furthermore, chlamydial STIs in 80% of women and 50% of men produce little to no symptoms, and thereby remain undetected and untreated. Unfortunately, untreated infection can lead to tubal infertility and ectopic pregnancy. Although these infections can be detected by screening sexually active individuals, widespread screening is not routinely performed. An effective alternative would be the development of a vaccine. However, traditional approaches to vaccine development have been unsuccessful, simply because we do not yet understand the immunobiology of Chlamydia. My research has been focused on gaining that understanding, such that we might someday be able to prevent chlamydial infection. Chlamydial infection triggers the production of a variety of immunomodulatory molecules, collectively known as cytokines. Interferon-gamma, a cytokine produced in response to infection, induces several antimicrobial mechanisms, including the breakdown of tryptophan by indoleamine dioxygenase (IDO). Activation of IDO rapidly depletes intracellular tryptophan, thereby starving tryptophan-dependent Chlamydia of an amino acid it requires for protein synthesis. While this works effectively in tissue culture, the fact that chlamydial infections are widespread and often asymptomatic suggests that Chlamydia are somehow evading this immunological defense mechanism. Currently, the goal of my laboratory is to determine how Chlamydia evades destruction by IDO.