Trichomonas vaginalis extracellular vesicles suppress IFNε-mediated responses driven by its intracellular bacterial symbiont Mycoplasma hominis

• 成果类型: Article
• 署名作者: Kochanowsky, Joshua A.; Betts, Emma L.; Encinas, Gabriel; Amoah, Johnson; Johnson, Patricia J.
• 署名单位: University of California System; University of California Los Angeles; University of Arizona
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-8460
• DOI: 10.1073/pnas.2508297122
• 发表日期: 2025-07-01
• 关键词: SEXUALLY-TRANSMITTED INFECTIONS; nf-kappa-b; interferon-epsilon; cervical-cancer; gene-expression; il-8 production; UNITED-STATES; PREVALENCE; association; chlamydia

摘要

Trichomonas vaginalis is a common, extracellular, sexually transmitted parasite which is often found in symbiosis with the intracellular bacterium Mycoplasma hominis (Mh), an opportunistic pathogen of the female reproductive tract. How this symbiosis affects infection outcomes and the host cell innate immune response is poorly understood. Here, we show that infection with T. vaginalis in symbiosis with M. hominis or M. hominis alone triggers a noncanonical type I interferon, interferon-epsilon (IFN epsilon), but infection with T. vaginalis alone does not. We also demonstrate that extracellular vesicles (TvEVs) produced by the parasite downregulate host cell IFN epsilon, counteracting this symbiont-driven response and elevating infection. We further demonstrate that IFN epsilon, a hormonally regulated cytokine produced in the human reproductive system, is protective against T. vaginalis cytoadherence and cytolysis of host cells. These studies provide insight into how a parasite and its bacterial symbiont work in concert to regulate host cell innate immune responses to drive infection.