In contrast, the number of monocyte/macrophages (ED2~ cells) was regulated by the changes in testosterone in the scrotal testis. Although there have been reports of direct actions of testosterone on macrophages, and monocytes in particular, the observation that the testosterone responsiveness of the ED2~ population was lost in the abdominal testis indicates that this particular action may be mediated via the seminiferous tubules. In the cryptorchid testis there also was a restorative effect of elevated testosterone on resident macrophage numbers, which was not observed in the scrotal testis. The explanation for this restoration is not apparent, but it presumably involves the seminiferous tubules. asthma inhalers
Altogether, these data are indicative of a minor indirect effect of testosterone on monocytes or macrophage maturation in the adult rat testis, which appears to be mediated via the seminiferous epithelium. Nonetheless, it is unlikely that testosterone is the major factor mediating the direct action of Leydig cells on the number of resident macrophages. Consequently, these results are consistent with data provided earlier for the immature testis indicating that Ley-dig cells regulate testicular resident macrophage development via a non-androgenic mechanism.