Pelvic inflammatory disease (PID) is defined as an infection of the endometrium, fallopian tubes, and adjacent structures that is caused by the ascension of microorganisms from the lower to upper genital tract The microorganism most convincingly associated with PID is Chlamydia trachomatis, and our proposal would provide the exciting opportinity for a discovery of the antigen-specific cell mediated immune resposes that are most strongly associated with protection against C. trachomatis infection as well as the elucidation of the antigen specifc immune responses correlated with containment of C. trachomatis infection to the lower genital tract. The 200 women enrolled into this longitudinal investigation will be recruited from an acute PID cohort (Project 1) and from a cohort of women who are at high risk for endocervical infection with C. trachomatis (Project 4). Completion of our investigation will allow: 1. Better understanding of the CD4 T cell antigen-specific responses that are most strongly associated with protection from C. trachomatis infection at enrollment. 2. Better elucidation of the CD4 T cell antigen-specific responses that are most strongly correlated with protection from incident C. trachomatis infection. 3. Identification of novel chlamydia-specific T cell responses that are most strongly associated with the decreased likelihood of ascension of C. trachomatis from the lower to upper genital tract.
Collection of this information will provide important new data regarding delineation of protective antigenspecific cell mediated immune responses and will provide critical input for C. trachomatis vaccine development.
|Barral, Romina; Desai, Ruchi; Zheng, Xiaojing et al. (2014) Frequency of Chlamydia trachomatis-specific T cell interferon-? and interleukin-17 responses in CD4-enriched peripheral blood mononuclear cells of sexually active adolescent females. J Reprod Immunol 103:29-37|
|Darville, Toni (2013) Recognition and treatment of chlamydial infections from birth to adolescence. Adv Exp Med Biol 764:109-22|
|Darville, Toni; Pelvic Inflammatory Disease Workshop Proceedings Committee (2013) Pelvic inflammatory disease: identifying research gaps--proceedings of a workshop sponsored by Department of Health and Human Services/National Institutes of Health/National Institute of Allergy and Infectious Diseases, November 3-4, 2011. Sex Transm Dis 40:761-7|
|Frazer, Lauren C; Scurlock, Amy M; Zurenski, Matthew A et al. (2013) IL-23 induces IL-22 and IL-17 production in response to Chlamydia muridarum genital tract infection, but the absence of these cytokines does not influence disease pathogenesis. Am J Reprod Immunol 70:472-84|
|Vicetti Miguel, Rodolfo D; Harvey, Stephen A K; LaFramboise, William A et al. (2013) Human female genital tract infection by the obligate intracellular bacterium Chlamydia trachomatis elicits robust Type 2 immunity. PLoS One 8:e58565|
|Taylor, Brandie D; Darville, Toni; Ferrell, Robert E et al. (2013) Racial variation in toll-like receptor variants among women with pelvic inflammatory disease. J Infect Dis 207:940-6|
|Riley, Melissa M; Zurenski, Matthew A; Frazer, Lauren C et al. (2012) The recall response induced by genital challenge with Chlamydia muridarum protects the oviduct from pathology but not from reinfection. Infect Immun 80:2194-203|
|Taylor, Brandie D; Darville, Toni; Ferrell, Robert E et al. (2012) Variants in toll-like receptor 1 and 4 genes are associated with Chlamydia trachomatis among women with pelvic inflammatory disease. J Infect Dis 205:603-9|
|Tuttle, Marie S; Mostow, Eliot; Mukherjee, Pranab et al. (2011) Characterization of bacterial communities in venous insufficiency wounds by use of conventional culture and molecular diagnostic methods. J Clin Microbiol 49:3812-9|
|Chavez, Jean M; Vicetti Miguel, Rodolfo D; Cherpes, Thomas L (2011) Chlamydia trachomatis infection control programs: lessons learned and implications for vaccine development. Infect Dis Obstet Gynecol 2011:754060|
Showing the most recent 10 out of 15 publications