Experimental orchitis was first produced by Voisin et al. (1951) by iso-and autosensitization in guinea pigs ( 1 ) , by Freund et al. (1954) in rats (2), and by Pokorna et d. (1963) in mice (3). Recently, Mancini, Andrada et d. (1965) were able to produce allergic orchitis in man (4). A group of four volunteer patients suffering from prostatic carcinoma was studied. Each of the four patients was immunized prior to surgical castration with testicular suspensions (autoimmunization and isoimmunization) . After a period of 3-8 weeks, two of the four patients developed patchy lesions in the contralateral testis consisting of congestion, serous edema and sloughing of germinal cells. Low titered circulating antibodies also appeared. To obtain a model for autoallergic orchitis closely related to man, an attempt was made to induce autoallergic orchitis in monkeys.
Materials and Methods. Animals.Eight adult male rhesus monkeys (Macaca mulat t a ) 5 years of age or older and weighing 15-20 lb were selected for these experiments. They were unilaterally orchiectomized (hemicastrated) and blood specimens were obtained. The histological picture of the testis was normal from all animals except one (Monkey no. 4) which presented arrest of spermatogenesis in about 50% of the tubules.Tissue extracts. The testicular material obtained from each experimental animal at the time of hemicastration, if not used immediately, was preserved at -40'. The glands were trimmed, washed in cold buffered saline, cut up and homogenized for 5 min in phosphate buffered saline, pH 7.2, by means of a Teflon homogenizer. Two ml of saline was
It is at present not clear whether alpha interferon (INF-α) can participate in the control of glucocorticoid blood levels through direct action on the adrenal gland. In this study, the possible action of INF-α on cortisol release by adrenal tissue was tested in vitro. Slices of normal human adrenals were incubated with INF-α for 3 h at 37°C in 95% air and 5% CO2. Cortisol release by adrenal tissue was stimulated by INF-α, showing a dose-response curve from 20 IU/ml, the lowest dose that gave a response, to a maximal dose of 60 IU/ml when the response reached a plateau. The effect of INF-α on cortisol liberation by adrenal tissue in vitro may be implied in neuroimmune regulatory interactions.
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