Interferon epsilon (IFNɛ) is a type I interferon originally discovered in female reproductive epithelia for its antiviral and antiproliferative properties. We recently demonstrated that IFNɛ is constitutively expressed by macrophages, Leydig cells, and meiotic and post-meiotic spermatogenic cells in the murine and human testis, and plays a protective anti-viral role in the murine male reproductive tract. Significantly, expression of IFNɛ in the testis emerged between day 20 and 25 of age in mice, indicating a specific role in sexually-mature males. Consequently, the role of IFNɛ in testicular steroidogenesis was examined.
The gross anatomy and histology of the testis, epididymis and seminal vesicles of adult (56 day-old) and juvenile (25 day-old) mice lacking IFNɛ (Ifne-/-) was compared to normal wild-type mice. Luteinising hormone (LH) and testosterone were measured in serum and testis extracts from adult mice by RIA. RNA-sequencing (RNAseq) was performed on whole-testis RNA from adult Ifne -/-mice and wild-type littermates.
Testicular, epididymal and seminal vesicle weights in Ifne-/-mice were not different from wild-type controls at 25 and 56 days of age, and no gross histological differences in Leydig cell morphology was observed. However, adult Ifne -/-mice displayed an approximately 50% reduction in serum testosterone compared to wild-type mice. Serum LH and intratesticular testosterone were not significantly altered. RNAseq analysis of adult Ifne-/-and wild-type mouse testes showed reduced expression of the key testicular steroidogenic genes, Cyp11a1, Cyp17a1 and Star. Cyp19a and Hsd3b1 were unaltered.
These data demonstrate a significant role for constitutive IFNɛ in supporting normal serum testosterone levels in adult mice, apparently by stimulating expression of the genes responsible for cholesterol mobilisation (Star), side-chain cleavage (Cyp11a1) and conversion of pregnenolone/progesterone into androgens (Cyp17a1). However, intratesticular testosterone, serum LH and seminal vesicle weights were not altered in mice lacking IFNɛ, and the precise mechanisms involved require further investigation.