Interferon epsilon is produced in the testis and protects the male reproductive tract against virus infection, inflammation and damage

PLoS Pathog. 2024 Dec 2;20(12):e1012702. doi: 10.1371/journal.ppat.1012702. eCollection 2024 Dec.

Abstract

The testis is a reservoir for viruses that can cause persistent infection and adversely affect male reproductive health, an observation commonly attributed to deficiencies in inducible antiviral defence mechanisms. In this study, we demonstrate that interferon-epsilon (IFNε), a type I interferon initially discovered in female reproductive epithelia, is constitutively expressed by meiotic and post-meiotic spermatogenic cells, Leydig cells and macrophages in mouse testes. A similar distribution pattern was observed in human testes. Mice lacking IFNɛ were more susceptible to Zika virus-induced inflammation and damage of the testis and epididymis compared to wild-type mice. Exogenous IFNε treatment reduced the viral infection burden in cultured human testicular cells by inducing interferon-stimulated gene expression, and reducing inflammatory gene expression and cell damage. Treatment was more effective when administered prior to infection. These data indicate a critical role for constitutively-expressed IFNɛ in limiting viral infection and inflammatory damage in the male reproductive tract.

MeSH terms

  • Animals
  • Genitalia, Male / metabolism
  • Genitalia, Male / pathology
  • Genitalia, Male / virology
  • Humans
  • Inflammation* / metabolism
  • Interferon Type I / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Testis* / metabolism
  • Testis* / pathology
  • Testis* / virology
  • Zika Virus
  • Zika Virus Infection* / immunology
  • Zika Virus Infection* / virology

Substances

  • Interferon Type I

Grants and funding

These studies were funded by a grant from the National Health and Medical Research Council of Australia (APP1184867 to MPH), grants from Monash University and the Deutsche Forschungsgemeinschaft (DFG) to the International Research Training Group (IRTG) on ‘Molecular pathogenesis of male reproductive disorders’ between JLU Giessen and Monash University (GRK 1871/2), the Victorian Government’s Operational Infrastructure Support Programme, and the Hudson Institute Science Innovation Seed Grant (ECR category, to RW and EDG). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.