Inflammation of the male reproductive tract is accepted as being an important etiological factor of infertility. Experimental autoimmune orchitis (EAO) is characterized by interstitial lymphomononuclear cell infiltration and severe damage of seminiferous tubules with germ cells that undergo apoptosis and sloughing. Because the blood-testis barrier (BTB) is relevant for the protection of haploid germ cells against immune attack, the aim of this study was to analyze BTB permeability and the expression of tight junction proteins (occludin, claudin 11, and tight junction protein 1 [TJP1]) in rats during development of autoimmune orchitis. The role of IL6 as modulator of tight junction dynamics was also evaluated because intratesticular content of this cytokine is increased in EAO rats. Orchitis was induced in Sprague-Dawley adult rats by active immunization with testicular homogenate and adjuvants. Control rats (C) were injected with saline solution and adjuvants. Untreated (N) rats were also studied. Concomitant with early signs of germ cell sloughing, a reduced expression of occludin and delocalization of claudin 11 and TJP1 were detected in the testes of rats with EAO compared to C and N groups. The use of tracers showed increased BTB permeability in EAO rats. Intratesticular injection of IL6 induced focal testicular inflammation, which is associated with damaged seminiferous tubules. Rat Sertoli cells cultured in the presence of IL6 exhibited a redistribution of tight junction proteins and reduced transepithelial electrical resistance. These data indicate the possibility that IL6 might be involved in the downregulation of occludin expression and in the modulation of BTB permeability that occur in rats undergoing autoimmune orchitis.

No abstract

Basement membranes from vascular and nonvascular canine tissue were analyzed chemically and structurally. Basement membranes which derive from different embryologic cell lines were qualitatively similar but differed quantitatively in their amino acid and carbohydrate composition. In terms of residues per 1000 residues anterior lens capsule contained hydroxylysine 32, hydroxyproline 99.5, and glycine 288, compared with 20, 83.8, and 230 residues, respectively, for Descemet's membrane. Glomerular, alveolar, and choroid plexus basement membranes contained hydroxylysine 24, 6.8, and 9 residues, hydroxyproline 65, 35, and 48 residues, and glycine 229, 222, and 235 residues, respectively. The carbohydrate content was high in all, ranging from 12.5 and, 10.5% in anterior lens capsule and Descemet's membrane to 10.25, 6.7, and 7.3% in basement membranes from the glomerulus, alveolus, and choroid

The aim of this study was to analyze whether di(2-ethylhexyl) phthalate (DEHP), a Sertoli and Leydig cell toxicant, is able to induce alterations in the expression of testicular gap and tight junction proteins. DEHP was administered by gavage (1 g/5 mL corn oil/kg body weight/day) to 25-day-old male Sprague-Dawley rats for 2 days (DEHP-27d) and control rats were treated with corn-oil vehicle for 2 days (C-27d); animals were killed 24 h after the last treatment. Testes of DEHP-27d rats showed different degrees of germ cell sloughing of seminiferous tubules (ST). No alterations of the blood testis barrier (BTB) by lanthanum tracer study were observed. ST of DEHP-27d rats showed a milder immunofluorescence and more restricted expression of connexin-43 (Cx43) in the adluminal and basal compartment compared to C-27d. In DEHP-27d rats, we found a discontinuous immunofluorescent (IF) pattern for zonula occludens (ZO-1), contrasting with the continuous IF profile observed in C-27d, and a delocalization of claudin-11. A decrease in Cx43 and ZO-1 and no changes in occludin expression were detected by Western blot in the testes of DEHP-27d rats. Results from 57-day-old rats treated with DEHP for 2 days and held for 30 days without treatment showed that the alterations in protein expression induced by DEHP are reversible. However, a delay of spermatogenesis compared to C-57d rats, occurred. Data demonstrated that DEHP does not impair BTB permeability but induces germ cell sloughing that might respond to a down regulation of Cx43 and ZO-1 that alters cell junction proteins.

No abstract