The Role of miR-135a in Immune Responses to Chlamydia Trachomatis

Chlamydia trachomatis (Ct) is a Gram-negative obligate intracellular pathogen and the leading cause of sexually transmitted infection (STI) worldwide despite effective antimicrobial therapy. Often asymptomatic in women, Ct induces immunopathology leading to reproductive sequelae including cervicitis, pelvic inflammatory disease (PID), ectopic pregnancy and infertility. The paradoxical involvement of antibiotics to prevent bacterial growth ultimately reduces natural immunity, and further increases STI incident rates. While, veterinary Ct vaccines exhibit short-term resistance requiring booster doses to maintain protection, repeat vaccinations is not desirable in humans. Over the last decade a role for microRNA (miRNA) in innate, and adaptive immunity has been established. Harnessing the intrinsic functionality of miRNA could enhance the effectiveness of protective immunity and eliminate the need for booster doses to confer memory. Previous observations by our group observed one such microRNA, i.e. miR-135a down-regulated in both upper and lower genital tract at day 6 and 12 post challenge with Chlamydia muridarum. Thus, we sought to determine the mechanistic role of miR-135a following Chlamydia infection. Concurrently, we devised two new and rapid methodologies which can further aid in enhancing our understanding the role of microRNA in immune response.