Infection with a sexually transmitted disease, by definition, often occurs in association with human seminal fluid. The role of seminal fluid in augmenting transmission of these diseases has not been fully explored. One of the major constituents of the seminal fluid of many species is prostaglandin E2 (PGE2). This compound has been demonstrated to act as an immunosuppressive agent, and recently has been described as decreasing specific cytokine and cellular responses. Several of these responses have been elicited during experimental infection of animals with Chlamydia trachomatis. In addition, PGE2 has been shown to increase retroviral activity in vitro. These findings suggest a role for seminal PGE2 in infection of a receptive sexual partner. Therefore, one of the specific aims of this project is to evaluate the effects of PGE2, a major component of human seminal fluid and an endogenously produced local hormone, on the response of the female genital tract to the common STD, C. trachomatis. Ultimately, this investigation may suggest therapies to block PGE2 receptors in the receptive sexual partner, reducing the risk of STD transmission. An additional benefit may be to direct further studies towards immunomodulatory therapies for chlamydial pelvic inflammatory disease (PID).

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Primate Research Center Grants (P51)
Project #
5P51RR000166-38
Application #
6116378
Study Section
Project Start
1999-05-01
Project End
2000-04-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
38
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of Washington
Department
Type
DUNS #
135646524
City
Seattle
State
WA
Country
United States
Zip Code
98195
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