CHARACTERIZING THE ROLE OF INNATE AND ADAPTIVE IMMUNE RESPONSES IN THE PATHOGENESIS OF CHLAMYDIA GENITAL TRACT INFECTION

Sexually transmitted infections with Chlamydia trachomatis are highly prevalent and can lead to irreversible tissue damage if infection ascends from the cervix to the upper reproductive tract. The goal of these studies was to determine key immune responses involved in either the development of oviduct pathology or protection from infection. Using the mouse model of Chlamydia genital tract infection, we determined that increased neutrophil recruitment and delayed apoptosis were associated with enhanced oviduct damage. Despite the important role of neutrophils in Chlamydia-induced tissue damage, we were unable to detect a central role for IL-17, IL-22, or IL-23 in neutrophil recruitment or the development of pathology. We found that IL-17 did promote Th1 immunity to infection but was not required for normal resolution of infection. Finally, we determined that expression of the adaptor molecule MyD88 by CD4+ T cells was required for efficient resolution of Chlamydia from the genital tract due to its role in enhancing the survival of these cells. These studies revealed that increased influx, survival, or activation of innate immune cells in the genital tract was associated with enhanced disease while prolonged survival of CD4+ T cells was associated with more efficient clearance of bacteria from the genital tract