? DESCRIPTION (provided by applicant) Chlamydia trachomatis (Ct), is the leading cause of bacterial sexually transmitted infections in the U.S., with increasing incidence rates over the las 10-15 years. A bench-to-bedside solution for a preventative vaccine for Ct is not available. Knowledge of inherent host molecular mechanisms that may influence host immunity will be helpful in improving down-selection of putative anti-Ct vaccine candidate(s). To this end, there is growing consensus on the role of small non-coding species of regulatory RNA, i.e. microRNAs (miRs) in critical processes including immunity and reproductive biology. Additionally, vaccination strategies or immunotherapy using miRs have now been established. Our recent report on the role of miR modulating host immunity and association studies on Ct-miR(s) collectively highlight the importance of these immune modulators in Ct infections and underscores the need to define their contribution in anti-Ct immunity. In this proposal, we plan toinvestigate specifically, the role of miR-182 in colonization of Chlamydia muridarum (Cm) via regulation of host protein, Alpha-2HS-Glycoprotein (AHSG) in the murine genital tract. Additionally, we plan to investigate the regulation of miR-182-AHSG in vaccinated mice where antigen (Ag)-specific CD4+T cells and interferon-? (IFN- ?) in accelerate Cm clearance from the genital tract. Taken together, this application aims at providing novel information on the role of miR-182 in chlamydial infections and modulation of miR-182 and its host targets by anti-Ct immunity.
|Effective start/end date||7/14/16 → 6/30/18|
- National Institutes of Health: $73,500.00