# Elucidating the role of IFN epsilon mediated type I IFN responses against Trichomonas vaginalis

> **NIH NIH F32** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2024 · $50,999

## Abstract

PROJECT SUMMARY / ABSTRACT
Trichomonas vaginalis (Tv) is a protozoan parasite that causes the most common non-viral sexually transmitted
infection (STI), trichomoniasis, world-wide. The rise in drug resistant strains of Tv, and an emerging appreciation
of the link between asymptomatic Tv infections with inflammation-driven pathologies demands better
understanding of this prevalent human infection. Notably, Tv infection has been linked to reproductive
complications, increased susceptibility to HIV, increased incidence of cervical cancer, and increased
aggressiveness of prostate cancer. Clinically relevant infection most commonly occurs in female reproductive
tract (FRT) where it must contend with the unique mucosal immune environment of the FRT. Interestingly in
contrast to other STIs, the detection rate of Tv is highest in peri- and post-menopausal women. Thus,
understanding how Tv subverts the host cell immune response, with a particular focus on the unique immune
environment of the FRT, will be key in attempts to prevent pathogenesis by the parasite. Over the past decade
our lab has shown that extracellular vesicles secreted by Tv (TvEVs) are internalized by human cells where they
can alter pathogenesis by altering cytokine secretion and increasing adherence of the parasite to its host cell.
Our lab and others have also shown that neutrophils (polymorphonuclear cells [PMNs]), the major immune cell
present at the Tv–host interface, kills Tv via a mechanism known as trogocytosis. Additionally, preliminary data
in our lab has shown that TvEVs down-regulate expression of a non-canonical, type I interferon, IFNε and that
pretreatment of prostate cells with IFNε is protective against Tv-mediated killing. Interestingly, IFNε, is known to
play an important role in protection of the FRT from bacterial and viral STIs. To elucidate the role of IFNε and
TvEVs we aim to: i) determine which step(s) in the IFNε-mediated type I IFN response is blocked by TvEVs and
ii) determine the role of IFNε and TvEVs during Tv infection of vaginal epithelial cells and interaction with PMNs.
The work proposed in this fellowship will increase our understanding of how TvEVs subvert an FRT specific
immune response mediated by IFNε that would otherwise be protective against the parasite.

## Key facts

- **NIH application ID:** 10998491
- **Project number:** 1F32AI186416-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Joshua Andrew Kochanowsky
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $50,999
- **Award type:** 1
- **Project period:** 2025-01-01 → 2025-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10998491

## Citation

> US National Institutes of Health, RePORTER application 10998491, Elucidating the role of IFN epsilon mediated type I IFN responses against Trichomonas vaginalis (1F32AI186416-01). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/10998491. Licensed CC0.

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