Genital tract infections with the obligate intracellular bacterial pathogen Chlamydia trachomatis cause a number of clinically distinct syndromes ranging from acute self-limiting infection to chronic conditions that can result in infertility. Control of chlamydial disease will likely depend on a multidisciplinary approach, including the development of immunoprophylactic or immunotherapeutic strategies. Because chlamydiae infect, replicate and cause disease at mucosal sites, an understanding of the importance and characteristics of mucosal immune responses in host immunity is needed. The long range goal is to obtain a detailed understanding of mucosal immune responses that confer immunity to chlamydial genital tract infection. The goal of this project is to use the murine model of chlamydial genital tract infection to begin to characterize mucosal immune responses that are elicited and which may contribute to immune protection. That goal will be achieved through 3 specific aims: 1) T and B cell subpopulations that predominate in local genital tract tissue during the course of infection will be identified and characterized using immunohistological and cytokine (ELISPOT) detection methodologies. 2) The role (s) of Th1 and Th2 type helper T cell responses in the resolution of infection will be defined using in vivo treatments with cytokines and anti-cytokine antibodies. 3) Immunoglobulin-deficient and interferon-gamma-deficient strains of gene knockout mice will be used to further characterize the importance of antibody and cell mediated responses in immunity to chlamydial genital tract infection. Results from these studies will contribute significantly to our understanding of the function of mucosal immune responses in acquired immunity to chlamydial genital tract infection.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI038991-03
Application #
2672632
Study Section
Bacteriology and Mycology Subcommittee 2 (BM)
Project Start
1996-06-01
Project End
2000-05-31
Budget Start
1998-06-01
Budget End
1999-05-31
Support Year
3
Fiscal Year
1998
Total Cost
Indirect Cost
Name
Montana State University Bozeman
Department
Microbiology/Immun/Virology
Type
Schools of Arts and Sciences
DUNS #
City
Bozeman
State
MT
Country
United States
Zip Code
59717
Morrison, Sandra G; Farris, Christina M; Sturdevant, Gail L et al. (2011) Murine Chlamydia trachomatis genital infection is unaltered by depletion of CD4+ T cells and diminished adaptive immunity. J Infect Dis 203:1120-8
Farris, Christina M; Morrison, Richard P (2011) Vaccination against Chlamydia genital infection utilizing the murine C. muridarum model. Infect Immun 79:986-96
Farris, Christina M; Morrison, Sandra G; Morrison, Richard P (2010) CD4+ T cells and antibody are required for optimal major outer membrane protein vaccine-induced immunity to Chlamydia muridarum genital infection. Infect Immun 78:4374-83
Han, Y; Morrison, R P; Cutler, J E (1998) A vaccine and monoclonal antibodies that enhance mouse resistance to Candida albicans vaginal infection. Infect Immun 66:5771-6