Dejucq N, Lienard M O, Guillaume E, Dorval I, Jégou B
GERM-INSERM U-435, Université de Rennes I, Campus de Beaulieu, Bretagne, France.
Endocrinology. 1998 Jul;139(7):3081-7. doi: 10.1210/endo.139.7.6083.
The testis is divided into two compartments: the seminiferous tubules and the interstitial tissue. The latter essentially consists of the blood and lymphatic vessels, testosterone-producing Leydig cells, and testicular macrophages. In the exploration of the testicular antiviral defense system, we initially searched for interferon (IFN) production by the seminiferous tubule cells. The site of virus entry into the testis is probably the interstitial compartment; thus, it is important to know whether and how the cells in this compartment are protected against viral infection. In addition, as germ cell precursors (spermatogonia) are only partially protected by the blood-testis barrier, it was important to explore the antiviral capability of these cells. In this study we searched for IFN production by Leydig cells, testicular macrophages, and spermatogonia after exposure to Sendai virus. We also investigated the effect of viral exposure on testosterone production by Leydig cells. Our results show that spermatogonia do not constitutively express IFNs and give a very poor response to the virus. In contrast, testicular macrophages constitutively produced type I IFNs, and this production was markedly stimulated by Sendai virus. Leydig cells produced twice as much type I IFNs as testicular macrophages after viral exposure, and they were the only cells producing both IFNalpha and -gamma, with these IFNs being dramatically induced/ increased in response to exposure to the virus. Furthermore, incubation of Leydig cells with the Sendai virus stimulated testosterone production. In conclusion, this study further establishes the topography of IFN expression within the testis. This allows us to hypothesize that the potential antiviral system represented by Leydig cells and, to a lesser extent, by macrophages plays a key role in protecting both androgen production and spermatogenesis.
生精小管和间质组织。后者主要由血管、淋巴管、产生睾酮的睾丸间质细胞和睾丸巨噬细胞组成。在探索睾丸抗病毒防御系统时，我们首先研究了生精小管细胞是否产生干扰素（IFN）。病毒进入睾丸的部位可能是间质部分；因此，了解该部分的细胞是否以及如何免受病毒感染非常重要。此外，由于生殖细胞前体（精原细胞）仅部分受到血睾屏障的保护，因此探索这些细胞的抗病毒能力也很重要。在本研究中，我们检测了睾丸间质细胞、睾丸巨噬细胞和精原细胞在接触仙台病毒后IFN的产生情况。我们还研究了病毒暴露对睾丸间质细胞睾酮产生的影响。我们的结果表明，精原细胞不组成性表达IFN，对病毒的反应也很差。相比之下，睾丸巨噬细胞组成性产生I型IFN，这种产生受到仙台病毒的显著刺激。病毒暴露后睾丸间质细胞产生的I型IFN是睾丸巨噬细胞的两倍，并且它们是唯一同时产生IFNα和-γ的细胞，这些IFN在接触病毒后被显著诱导/增加。此外，将睾丸间质细胞与仙台病毒一起孵育可刺激睾酮的产生。总之，本研究进一步确定了睾丸内IFN表达的格局。这使我们能够假设，由睾丸间质细胞以及在较小程度上由巨噬细胞代表的潜在抗病毒系统在保护雄激素产生和精子发生方面起关键作用。
