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PubMed1984

The dark mink: a model of male infertility.

Breeding mink for a fine dark fur has coselected male infertility, which may be manifest at the onset of breeding (primary infertility) or after one or more fertile breeding seasons (secondary infertility). Mink with primary infertility have low LH and testosterone levels. However, they respond to exogenous GnRH with increases in LH production and in the number and size of LH and FSH positive gonadotropes in the anterior pituitary. Exogenous human CG also induces testosterone secretion. Thus, mink with primary infertility are probably defective in GnRH secretion, which is due either to abnormal hypothalamic function or its control mechanisms. Autoimmune orchitis with testicular immune complexes are frequent in mink with secondary infertility, suggesting an autoimmune etiology. In contrast, fertile dark mink and fertile mink with the opaline and pastel fur have normal serum LH and testosterone levels; their testes are also normal. In mink with secondary infertility, the frequency and degree of orchitis and testicular immune complexes increased from March (peak sexual activity) to April (onset of testicular regression). Thus, testicular autoimmunity most likely develops during testicular regression. Antisperm antibodies also increased in frequency during testicular regression in the fertile dark mink and in dark mink with primary and secondary infertility. Thus, antisperm antibody per se is insufficient to induce autoimmune orchitis. It is concluded that the infertile mink is a useful model of human male infertility, involving both endocrinological and immunological mechanisms.

Animals↗

PubMed2000

Expression and regulation of the CXC-chemokines, GRO/KC and IP-10/mob-1 in rat seminiferous tubules.

Testicular inflammation is classically observed in the pathogenesis of viral and bacterial infection or tumoral invasion. In these situations, leukocyte infiltration is generally encountered. GRO/KC (growth-related oncogene) and IP-10/mob-1 (IFN-gamma-inducible protein) are two CXC-chemokines which attract neutrophils and activated T lymphocytes, respectively, have been studied for their ability to participate to testicular inflammation (orchitis). In the present work, using Northern blot and immunocytochemistry, we aimed to investigate whether GRO/KC and IP-10/mob-1 are produced within the seminiferous tubules of the testis and if these chemokines are induced by a number of pro-inflammatory cytokines and lipopolysaccharides (LPS). Our results show that GRO/KC and IP-10/mob-1 mRNAs were never found in germ cells, whether they were stimulated or not. In contrast, GRO/KC mRNA was expressed by isolated peritubular cells when stimulated by interleukin-1 alpha and beta (IL-1 alpha and IL-1 beta) or LPS and to a lesser extent by tumor necrosis factor-alpha (TNF-alpha) and by Sertoli cells when the latter were stimulated by rIL-alpha and rIL-1 beta and to a lesser extent by TNF-alpha and LPS. Moreover, IP10/mob-1 transcripts were strongly induced in peritubular cells by interferon-alpha (IFN-alpha) and IFN-gamma, whereas, in isolated Sertoli cells, INF-alpha and TNF-alpha were the only potent inducers. The kinetics of GRO/KC and IP-10/mob-1 mRNA expression by peritubular and Sertoli cells (significant stimulation as early as 1 hour and 4 hours post-exposure to the stimuli, respectively) are compatible with the hypothesis of a rapid mobilisation of these cells in an inflammatory process. Moreover, the dose-dependent effects of pro-inflammatory cytokines to induce a chemokine response were compatible with a high sensitivity of peritubular and Sertoli cells in orchitis. In conclusion, this present study shows that 2 CXC-chemokines, GRO/KC and IP10/mob-1, are produced by testicular somatic cells of seminiferous tubules, strongly indicating a likely role of these chemokines in the accumulation of neutrophils and T lymphocytes during orchitis of various origins.

Animals↗

PubMed1998

Urological manifestations of HIV infection.

HIV-1 disease is associated with many infectious and neoplastic complications. This is particularly true of the genitourinary tract, where high rates of renal disease, neoplasms, voiding and erectile dysfunction, hematuria, opportunistic genitourinary infections, and epididymo-orchitis are found in HIV-1-infected individuals. Recent experience at Ben Taub General Hospital (Houston, TX) shows that men requiring admission to the urologic service for treatment of genitourinary disorders have high rates of HIV-1 seropositivity, particularly in the setting of epididymo-orchitis, where 21 of 106 (20%) were found to be HIV-1 infected. These men were significantly more likely to require surgical treatment and to harbor resistant bacteria in infected tissues. Importantly, for 15 of 21 HIV-1-infected men, epididymo-orchitis was the first clinical manifestation of HIV-1 disease, and 6 were first found to be HIV-1 seropositive during that admission. Our experience illustrates the critical importance of screening for HIV-1 infection in the setting of genitourinary disease.

Adolescent↗

PubMed2000

Gray-scale and power doppler sonographic appearances of acute inflammatory diseases of the scrotum.

PURPOSE: We describe the spectrum of gray-scale and power Doppler sonographic appearances in inflammatory scrotal diseases. METHODS: Twenty-five patients ranging in age from 3 to 69 years underwent gray-scale and power Doppler sonography with multifrequency transducers of 7-9 MHz or 10-13 MHz. In addition, color Doppler and power Doppler findings were compared in 7 cases. RESULTS: In all 5 prepubertal patients, power Doppler imaging demonstrated hyperemia associated with epididymitis and, in some cases, orchitis. Among the 20 pubertal and adult patients, power Doppler imaging revealed increased vascularity associated with spermatic cord involvement, epididymitis, orchiepididymitis, or orchitis. Enlargement and heterogeneity of the epididymis and/or testis were seen in 11 patients, with vas efferens ectasia in 3 patients. Abscess formation and testicular infarction were easily depicted by power Doppler imaging. In 5 cases total, hyperemia was the only sonographic finding of inflammation. In the comparison between color and power Doppler imaging, a subjective increase in the number and length of vessels was seen with power Doppler imaging. CONCLUSIONS: Power Doppler imaging is an easy and fast Doppler modality for evaluating inflammatory conditions of the scrotum and proved especially useful in cases with no gray-scale sonographic anomalies, in prepubertal patients, and in patients with abscesses or ischemic lesions.

Acute Disease↗

PubMed1999

Effect of long-term vasectomy on seminiferous tubules in the guinea pig.

The little previous work on the influence of vasectomy on the guinea pig testis has given controversial results. One group reports that the guinea pig suffers autoimmune orchitis while others claim damage may be mechanical. To clarify the issue, this study compares the morphology of seminiferous tubules 3 years after left unilateral vasectomy (8 guinea pigs) and control sham operation (6 animals). Grossly, left and right testes following left-sided vasectomy were similar to controls and not significantly different in weight. On histology, left and right experimental testes and the control material showed various degrees of seminiferous tubular degeneration, including intraepithelial vesicle formation, loss of germ cells and intraluminal macrophages. Although vesicle formation was striking in most testes, quantitative analysis indicated that it was more frequent in the ipsilateral testis following unilateral vasectomy. It seems that vasectomy had exacerbated an age-related phenomenon. Lymphocytic infiltration was seen in five of the left testes following vasectomy, in two of the corresponding right testes, but in none of the controls. Two vasectomized left testes, however, showed atrophic changes but no lymphocytic invasion. The results suggest that autoimmune orchitis follows vasectomy but that it may not be the primary cause of degeneration. Attempts to gain positive evidence for mechanical damage, however, were inconclusive.

Analysis of Variance↗

PubMed2006

Development of testicular inflammation in the rat involves activation of proteinase-activated receptor-2.

Mast cells are involved in early events crucial to inflammation and autoimmune disease. Recently, proteinase-activated receptor-2 (PAR(2)), a G-protein coupled receptor important to injury responses, was shown to be activated by mast cell tryptase. To investigate whether mast cells and PAR(2) are involved in the development and/or aggravation of testicular inflammation, we studied acute and chronic inflammatory models in the rat. In normal testes, PAR(2) was detected immunohistochemically in macrophages, in peritubular cells (PTCs) and in spermatid acrosomes. In experimentally induced autoimmune orchitis (EAO), PAR(2) was strongly upregulated in macrophages and peritubular-like cells, forming concentric layers around granulomas. Mast cells increased 10-fold in number, were more widely distributed throughout the interstitial tissue, and were partially degranulated. Isolated PTCs expressed functional PAR(2), responded to PAR(2) activation by phosphorylating extracellular signal-regulated kinases 1/2 (ERK1/2) and activating protein kinase c, and increased intracellular Ca(2+) concentrations as well as monocyte chemoattractant protein-1 (MCP-1), transforming growth factor beta(2) (TGFbeta(2)), and cyclooxygenase-2 (COX-2) mRNA expression. Expression of these inflammatory mediators, together with iNOS, also increased significantly in testes 50 days after EAO. In vivo, expression of cytokines and inflammatory mediators was upregulated after injection of recombinant tryptase (MCP-1, TGFbeta(2), and COX-2) and a specific PAR(2) peptide agonist (MCP-1, TGFbeta(2)) in the testis after 5 h. These results suggest that PAR(2) activation elicited on PTCs by mast cell tryptase contributes to acute testicular inflammation and that this pathogenetic mechanism may also play a role in autoimmune orchitis.

Acute Disease↗

PubMed1991

The effects of experimental Trypanosoma (Trypanozoon) (brucei) evansi infection on the fertility of male goats.

The effects on the fertility of small East African male goats of intravenous infection with Trypanosoma (t) (b) evansi were studied. Six infected bucks developed erratic, low but persistent parasitaemia, the packed cell volume dropped gradually but significantly (p less than 0.001) and they became emanciated. Half of these bucks developed clinical orchitis. Two bucks died of the disease during the experiment. Semen from all the infected bucks deteriorated in quality and quantity and those with clinical orchitis became totally aspermic. Spermatozoal abnormalities and the number of dead spermatozoa rose significantly. Later in the disease, the testicles of the infected bucks atrophied. Histologically, the testicles from the infected animals became devoid of spermatozoa, the testicular blood vessels contained microthrombi and there was infiltration of inflammatory cells. Subsequently, diffuse calcification set in, with calcium deposits obliterating most of the seminiferous vesicles and ducts and also the epididymal ducts.

Animals↗

PubMed1987

Recurrent episodes of testicular swelling preceding Henoch-Schönlein purpura by 11 months.

We report an unusual presentation of Henoch-Schönlein purpura in a 4-year-old boy. He presented with two isolated episodes of tender testicular swelling, and 11 months after the first episode developed a full blown picture of Henoch-Schönlein purpura accompanied by orchitis. A latent period of orchitis preceding Henoch-Schönlein purpura of this duration has not been described previously and its clinical implications are discussed.

Child, Preschool↗

PubMed1990

Role of testicular autoantigens and influence of lymphokines in testicular autoimmune disease.

The present data on testicular autoimmune disease suggest that CD4+ helper type T cells are responsible for adoptive transfer of murine experimental autoimmune orchitis (EAO). In passive EAO, the earliest lymphoid cell infiltration is confined to terminal segments of seminiferous tubules. Both orchitis and vasitis develop. In active EAO, any location in the testis is affected, frequently involving subcapsular seminiferous tubules. The location of maximum histopathology in passive EAO coincides with the site in the normal testis that expresses maximal Ia. Demonstration of IgG in the testis after immunization with testicular antigens or after transfer of sera from orchiectomized mice immunized with testis shows that autoantigens are present on the germ cells outside the Sertoli cell barrier, suggesting the existence of dynamic protective mechanisms against immune responses to the non-sequestered autoimmunogenic germ cells in normal individuals.

Animals↗

PubMed2005

A complication of brucellosis: epididymoorchitis.

BACKGROUND: Epididymoorchitis is the most frequent genitourinary complication of brucellosis. METHODS: This prospective study was conducted between February 2001 and January 2004, prospectively. Male patients diagnosed with brucellosis were included in this study and evaluated for testicular involvement. RESULTS: Epididymoorchitis was detected in 17 out of 134 (12.7%) male patients with brucellosis. Mean age of the patients was 36.9+/-7.1 years. Twelve patients (70.6%) had acute, four patients (23.5%) had subacute, and one patient (5.9%) had chronic brucellosis. The most common symptoms were scrotal pain (94%) and swelling (82%). Eleven patients had unilateral epididymoorchitis, four had unilateral orchitis and two had unilateral epididymitis. A testicular abscess was detected in one patient. Sperm analysis was performed on 14 patients. Five patients had aspermia and eight had oligospermia. Combined antibiotic therapy was started and continued for 6-8 weeks. Orchiectomy was required for two patients and granulomatous orchitis was detected in the resected specimens. Relapse occurred in only one patient. Three patients had permanent oligospermia and one patient had permanent aspermia after the antibiotic therapy. Younger age, high C-reactive protein level and blood culture positivity were statistically significant differences between the patients with and without epididymoorchitis. CONCLUSIONS: Brucellosis should be considered in the diagnosis of scrotal diseases in endemic areas. A conservative approach is usually adequate for managing brucellar epididymoorchitis. However, infertility problems may develop in these patients. Well-designed further investigations are needed to explain the relationship between brucellar epididymoorchitis and infertility in man.

Adult↗

PubMed2006

Endoscopic treatment of vesicovasal and vesicoureteral reflux in infants with persisting mesonephric duct.

PURPOSE: We present a minimally invasive endoscopic approach for the treatment of persisting mesonephric duct in male infants. MATERIALS AND METHODS: Five male infants 2 to 8 months old were referred with a history of recurrent sepsis, epididymo-orchitis and anorectal malformation that was treated elsewhere with initial colostomy. All infants had edematous unilateral testes, fever and poor feeding. Urine and blood cultures yielded the same microorganisms. All infections occurred while the infants were on regimens of prophylactic antibiotics. Comprehensive urological evaluations confirmed ipsilateral renal agenesis, sacral hypoplasia (3 patients), high anorectal malformation, and vesicovasal and vesicoureteral reflux. RESULTS: All 5 infants underwent urethrocystoscopy under general anesthesia. The ectopic persisting mesonephric duct entered the bladder neck and proximal prostatic urethra. Injection of 0.4 to 0.7 ml Urocol, used as a bulking agent, was administered submucosally at the opening of the persisting mesonephric duct. In 1 patient the orifice of the anomalous duct was not found during urethrocystoscopy, and ipsilateral vas ligation by titanium clips was performed. The results in the remaining 4 patients were excellent, and no further episodes of epididymitis were observed during a mean followup of 30 months. CONCLUSIONS: The diagnosis of persisting mesonephric duct should be considered in a male child with anorectal anomalies and recurrent epididymo-orchitis, and can be confirmed by radiological studies and cystoscopy. Endoscopic treatment of this anomaly should be considered first line therapy in these patients. However, surgical intervention is mandatory for children not responding to the procedure.

Cystoscopy↗

PubMed1988

Etiology of acute scrotum in 100 boys with regard to age distribution.

A review of 100 boys less than 15 years old who were hospitalized for an acute scrotum revealed that the most common causes of the disorder were testicular torsion, including torsion of the spermatic cord (42 per cent) and torsion of the appendages (32 per cent). The remaining 26 per cent of the cases were owing to idiopathic scrotal edema (8 per cent), epididymitis and orchitis (6 per cent each), and incarcerated hernia and acute hematocele (3 per cent each). The age distribution of these children was biphasic, with the highest frequency in newborns (with exclusively extravaginal torsion) and in boys 13 years old, whereas in boys with appendiceal torsion the single peak frequency was at age 10 years. While idiopathic scrotal edema occurred in children less than 7 years old and orchitis in patients more than 12 years old, epididymitis was observed in young boys and those of pubertal age.

Acute Disease↗

PubMed1995

Elucidation of autoimmune disease mechanism based on testicular and ovarian autoimmune disease models.

This paper describes several selected models of autoimmune disease of the gonads. Based on these findings, I have reviewed current knowledge concerning the tolerance mechanisms that normally prevent gonadal autoimmunity, the potential events that can overcome such mechanism to trigger autoimmune diseases. In addition we also summarize the immunopathology of orchitis and our understanding of the mechanisms responsible for the immunopathology of the disease. Recent studies indicate that pathogenic T cells capable of eliciting autoimmune diseases in these organs develop in both the neonatal and adult thymuses and they persist in the normal peripheral immune system. However, the function of the pathogenic T cells in adult mice is normally under the control of regulatory T cells which maintain peripheral tolerance, and important phenotypic differences are being defined between these two functional CD4+ T cell subsets. When the clonal balance of these T cell subsets is tipped in favor of pathogenic T cells, autoimmune diseases of the gonads could ensue. Pathogenic T cells responsible for autoimmune oophoritis can be activated through stimulation by non-ovarian peptides that cross-react with self ovarian peptides at the level of the T cell receptor. This novel form of antigen mimicry depends in part on the sharing, between unrelated peptides, the few critical amino acids required for activation of pathogenic T cells. Antibodies can bind to the ovarian target antigens during the development of autoimmune orchitis and autoimmune oophoritis. However, the precise role of antibody in these autoimmune diseases has not been critically explored. In this study, I have described a novel mechanism of autoantibody induction. Immunization of female mice with a pure T cell peptide from ZP3 can lead to the production of antibodies against ZP3 domains outside the immunogenic ZP3 peptide. Evidently, endogenous antigens from normal and pathologic ovaries may reach peripheral immune tissues, and provide the antigenic stimulus to trigger an autoantibody response. This occurs at the same time when activation of ZP3 specific T cells is detected, and it is not simply a consequence of tissue injury. Importantly, the autoantibodies react with native antigenic determinants, and are potentially important in autoimmune disease pathogenesis.

Animals↗

PubMed1992

[MR tomography in testicular processes. The significance of Gd-DTPA enhanced sequences in comparison with plain T2-weighted sequences].

The value of T1-weighted sequences after intravenous administration of Gd-DTPA and of T2-weighted sequences was compared in 43 patients suspected of having scrotal abnormalities. T2-weighted sequences gave better demonstration of the tunica albuginea and better contrast between tumor and parenchyma. The two techniques were equally sensitive for demonstrating testicular tumors but orchitis was better demonstrated on the contrast enhanced sequences. Motion artifacts were less marked in the T1-weighted sequences with contrast enhancement. In selected cases, contrast enhancement may be a valuable addition to native protocols. Our experience has indicated that MRI provides specific findings in cases of orchitis which are clinically atypical; this facilitates the decision to conservative treatment and prevents unnecessary exploration of the testes.

Adolescent↗

PubMed1959

A histologic study of the auto-allergic testis lesion in the guinea pig.

The auto-allergic lesion in guinea pigs inoculated with homologous testis plus the Freund adjuvant was investigated histologically. The lesion was found to consist of disseminated foci of perivenous inflammation, lymphocytes and histiocytes predominating in the cellular infiltrate, with invasion of epididymal, rete, and seminiferous tubules and destruction of tubular contents. Guinea pigs up to 800 gm. showed a rapidly progressing diffuse hypo- or aspermatogenesis, which appeared to be secondary to the inflammatory disease. In these animals, the process resolved leaving an atrophic testis with few or no indications of the preceding inflammation and fibrotic scarring only in the rare instances in which actual necrosis of connective tissue elements had occurred. In 1200 gm. animals there was no general hypospermatogenesis and the late findings were limited to foci of aspermatogenesis. This disease then is an experimental auto-allergic orchitis followed by testicular atrophy without scarring. Its morphologic similarity to mumps orchitis and to sterility with "germinal cell aplasia" in man is commented on.

Animals↗

PubMed1985

Organ-specific autoimmune diseases induced in mice by elimination of T cell subset. I. Evidence for the active participation of T cells in natural self-tolerance; deficit of a T cell subset as a possible cause of autoimmune disease.

Organ-specific autoimmune diseases such as oophoritis, gastritis, thyroiditis, and orchitis were induced in female or male nude (nu/nu) mice by the transfer of nu/+spleen cells from which particular Lyt T cell subset(s) had been removed: nu/+spleen cells treated with anti-Lyt-1 plus complement (C) caused disease in recipient nude mice; anti-Lyt-2 plus C-treated spleen cells, in contrast, did not. The cells responsible for disease induction are believed to be Thy-1+, Lyt-1-, 2,3- (Thy-1, Lyt-1, 2,3), since spleen cells treated with mixed antisera, including anti-Lyt-1 and anti-Lyt-2, plus C, could induce the disease with almost the same incidence as anti-Lyt-1 plus C-treated cells (oophoritis 50%, gastritis 25%, thyroiditis 10-20%, and orchitis 40%). Cells treated with mixed antisera of anti-Thy-1, anti-Lyt-1, and anti-Lyt-2, plus C, could not induce autoimmune disease. Each induced autoimmune disease could be adoptively transferred to other nude mice via spleen cells, with resulting histological lesion of corresponding organs and development of specific circulating autoantibodies. Since anti-Thy-1 plus C treatment of donor spleen cells abrogated the capacity to transfer the disease, we conclude that T cells are required as effector cells, and that these may develop from Lyt-1-, 2,3- cells. Lyt-1+, 2,3- cells were demonstrated to have suppressive activity upon the development of the diseases; induction of autoimmunity was completely inhibited by the cotransfer of Lyt-1+, 2,3- cells with Lyt-1-, 2,3- cells. When anti-Lyt-2 plus C-treated cells (i.e., Lyt-1+, 2,3- and Lyt-1-, 2,3- cells) were mixed with anti-Lyt-1 and anti-Lyt-2 plus C-treated cells (i.e., Lyt-1-, 2,3- cells) in various ratios, then transferred to nude mice, the development of each autoimmune disease was clearly inhibited, even by small doses of Lyt-1+, 2,3- cells. The autoimmune disease we were able to induce was quite similar to human organ-specific autoimmune disease in terms of the spectrum of organs involved, histopathological features, and the development of autoantibodies to corresponding organ components (oocytes, parietal cells, thyroid colloid, including thyroglobulin, and sperm).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2003

Experimental inoculation of the adult rat testis with Sendai virus: effect on testicular morphology and leukocyte population.

BACKGROUND: Surprisingly little is known about the interactions between viruses and the male uro-genital tract. These are important, as viral testicular orchitis, induced by mumps or human immunodeficiency virus (HIV) infection for example, can lead to sterility. Moreover, semen is an essential vector in the propagation of sexually transmissible viral diseases. Here, we studied the effects of testicular infection with Sendai virus, a virus related to mumps virus, on the cellular distribution of viral particles and on testicular morphology, with particular attention to the testicular leukocyte population. METHODS: At 5, 9, 11 or 24 h post-injection of Sendai virus through the scrotum, the testes were fixed for morphological and immunohistological studies. Localization of virus particles and numeration of leukocytes were performed using specific antibodies and morphological criteria. RESULTS: As early as 5 h post-injection, a rapid and massive infiltration of leukocytes was observed in the interstitial tissue. The peritubular cell layer and the most external part of the basal portion of the seminiferous tubules were altered. The virus was diffusely located within the interstitial tissue 9 h following the injection whereas, after 24 h, viral proteins were restricted to the cytoplasm of infiltrated leukocytes. The number of leukocytes increased with time post-injection. Thus, 24 h post-injection, CD3+ T-cell number was 3-fold higher, ED1+ monocyte number was 4-fold higher and polynuclear cell number was 600-fold higher than in the control testes (P<0.001 all observations). In contrast, the population of resident macrophages was unaffected by Sendai virus. CONCLUSIONS: Testicular viral infection causes inflammation including rapid recruitment of leukocytes. The experiments presented here provide a model for further studies on the etiopathology of viral orchitis, in particular that caused by mumps virus.

Animals↗

PubMed1983

Genetic susceptibility to testicular autoimmunity: comparison between postthymectomy and postvasectomy models in mice.

The genetic susceptibility was compared in six mouse strains to both postthymectomy (post-Tx) autoimmune orchitis, induced by thymectomy at Day 3, and postvasectomy (post-Vx) autoimmune testicular lesions, induced by bilateral vasectomy with ligation at 2 months of age. Results from mice examined at 4 months of age showed that the strain distribution of the post-Vx testicular lesion was similar to that of post-Tx orchitis. The SWR/J strain was susceptible, the DBA/1J, C57L/J, BALB/cJ and probably C57BL/10J strains were resistant, and the A/J strain was intermediate. Anti-sperm antibodies (IgG) were produced to varying degrees in all strains of vasectomized mice irrespective of the testicular lesion. Neither the development of the testicular lesion nor antibody formation was associated with the particular H-2 haplotypes of mice in either system. Neonatal thymectomy significantly enhanced anti-sperm antibody formation in the post-Vx system and resulted in a mild testicular atrophy in a resistant strain BALB/cBy. All these data suggest that a gene(s) outside the major histocompatibility complex may determine the genetic susceptibility to testicular autoimmunity, possibly at the testicular level.

Animals↗