Experimental Autoallergic Orchitis in Rhesus Monkeys

Abstract

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

Experimental Production of Autoimmune Aspermatogenic Orchitis in the Rabbit in Consequence of in situ Freezing of the Testis

“…The histologic sequelae of this response was perhaps, similar to that observed following inoculation with isologous or autologous testicular tissue in the guinea pig [1], rat [2], mouse [3], monkey [4], and human [5] and to the effects of thermal injury on the guinea pig testis [13]. Three of the four animals exhibiting histologic changes in their contra lateral testis showed evidence, as described above, of rather low or mod est levels of circulating antibodies to their own testis.…”

A Modified Leucocyte Migration Assay as Indicator of Malignant and Non-Malignant Gastric Mucosal Alteration

“…We conclude from this observa tion (1) that the occasionally observed reactivity of cancer patients' leucocytes with normal gastric mucosal extracts is due to a weak sensitization against prod ucts of normal mucosal cell decay, occurring with progressing tumour growth, and (2) that the reactivity of patients with non-malignant gastric diseases with tumour extracts probably is due to sensitization against normal mucosal cell antigens, which will be found to some extent also in tumour extracts. The possibility of an immune reaction against normal mucosal cell antigens in gastric disease was experimentally established by a study with rhesus monkeys (2), where monkeys injected with an extract of gastric mucosal cells developed a humoral as well as a cellular immune response against gastric mucosal cell antigens together with a multifocal gastritis with atrophy. This hypothesis as cribing LM reactivity of patients with non-malignant gastric diseases to sensitiza tion against normal mucosal cell components is in line with a report of LM reactivity of patients with Crohn's disease and ulcerative colitis (6).…”

Postinflammation stage of autoimmune orchitis induced by immunization with syngeneic testicular germ cells alone in mice

“…[9][10][11][12] EAO has been induced in several animals, including monkey, guinea pig, rabbit, rat, and mouse, and is characterized by T-cell-dependent lymphocytic infl ammation and damage to the seminiferous tubules, i.e., sloughing and apoptosis of testicular germ cells (TGC). [13][14][15][16][17] We previously showed that EAO could be produced in both A/J and C3H/ He mice at a very high incidence by two subcutaneous injections of viable syngeneic TGC on days 0 and 14 without the use of any adjuvant. 11 In this EAO model, lymphocytic infi ltration consistently starts around the tubuli recti at around day 30, and then gradually and chronically spreads to the peripheral seminiferous tubules with disturbance of spermatogenesis for more than 120 days.…”