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and -
in Testicular Interstitial Tissue and Spermatogonia of the Rat1
GERM-INSERM U-435, Université de Rennes I, Campus de Beaulieu, 35 042 Rennes, Bretagne, France
Address all correspondence and requests for reprints to: Dr. Bernard Jégou, GERM-INSERM U-435, Université de Rennes I, Campus de Beaulieu, 35 042 Rennes Cedex, Bretagne, France. E-mail: bernard.jegou{at}rennes.inserm.fr
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 IFN
and -
, 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.
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