Extracellular vesicles of Trichomonas vaginalis suppress IFNϵ-mediated protection against host cell cytolysis

Trichomonas vaginalis is a commonly acquired sexually transmitted infection (STI) often found in symbiosis with the intracellular bacterium Mycoplasma hominis, an opportunistic pathogen of the female reproductive tract associated with bacterial vaginosis. How this symbiosis influences infection outcomes, and the host cell’s innate immune response, is still poorly understood. Here we show that extracellular vesicles of T. vaginalis downregulate a noncanonical type I interferon, interferon-epsilon, and suppress type I interferon responses. Transcriptomic analysis shows that infection with T. vaginalis in symbiosis with M. hominis or M. hominis alone upregulates genes involved in the type I IFN response, but infection with T. vaginalis alone does not. Finally, we show that interferon-epsilon stimulation is protective against cytoadherence and cytolysis of host cells by T. vaginalis and increases the ability of neutrophils to kill the parasite. These studies provide insight into the innate immune response caused by a common STD and its bacterial symbiont.