Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen that causes Fallopian tube inflammation and subsequent tubal infertility in women. Currently, more than 2 million young adults are infected and the annual cost of complications exceeds $2 billion, making chlamydia infection a huge public health problem.
Chlamydia spp. are obligate intracellular pathogens that replicate inside an inclusion within infected cells. A Th1-dependent adaptive immune response is required for effective eradication of chlamydial infection. Primarily, an innate immune response to infection involves up regulation of a wide assortment of genes (including proinflammatory cytokines such as TNFa, IFN-b, IL-1b and IL-6) by the infected cells, which contribute to the development of oviduct pathology in the mouse model.
The research in Dr. Uma Nagarajan's laboratory is mainly focused on understanding the innate immune responses to chlamydial infection and its role in genital tract pathology. Specifically, the researchers are interested in delineating pathogen recognition by the host, signaling pathways that lead to the induction of innate immune cytokines in vitro and their downstream cellular effects in vitro and in vivo.
Current projects in the laboratory examine the mechanisms of type I IFN and IL-1 induction during chlamydia infection, with the overall hypothesis that cell death pathways driven by these cytokines result in a cascade of inflammatory events resulting in tissue damage. The reseachers work in close collaboration with Toni Darville, MD, Catherine O Connell, PhD, and Xiaojing Zheng, PhD, in UNC Children's Division of Pediatric Infectious Diseases to understand chlamydial pathogenesis and translate the findings in the mouse model to human disease.