Disease relevance of Orchitis

• None of 24 sera from men with seminomas and none of 5 sera from men with orchitis had elevated SP1 [1].
• 5HT, the immediate stimulus of testicular CRF secretion, is released during stress and is locally increased in the testis in pathological conditions associated with impaired testicular function (i.e., orchitis, varicocele) [2].
• We report 8 patients with Wegener granulomatosis (WG) who suffered from symptomatic urogenital involvement including acute urinary retention related to prostatitis, orchitis, ureteral stenosis, bladder pseudotumor, and penile ulceration [3].
• Hence, the aging AROM+ males present with a phenocopy of inflammation-associated infertility in men, providing a model for further studies on the putative link among estrogens, orchitis, and infertility [4].
• The serum CRP titers were significantly higher in the patients with orchitis than in those with meningitis [5].

High impact information on Orchitis

• In two rabbits with higher levels of circulating antisperm antibodies and severe orchitis, granular deposits of IgG and C3 were also present in renal glomeruli [6].
• Acute orchitis in familial Mediterranean fever [7].
• Multiple loci govern the bone marrow-derived immunoregulatory mechanism controlling dominant resistance to autoimmune orchitis [8].
• Adeno-associated virus-mediated human IL-10 gene transfer suppresses the development of experimental autoimmune orchitis [9].
• 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) [10].

Chemical compound and disease context of Orchitis

• Ciprofloxacin or clavulanic acid/amoxicillin was administered as bacterial orchitis could not be excluded at initial presentation [11].
• Thus, B. pertussis-induced sensitivity to histamine appears to play a more crucial role during the sensitization phase of autoimmune orchitis induction, rather than at the inflammatory or effector phase of the disease [12].
• Moreover, rats with orchitis had significantly increased testicular testosterone [13].
• The effects of the treatment with the immunosuppressant deoxyspergualin on the development of experimental autoimmune orchitis were studied [14].
• The increase in testicular steroidogenesis without a concomitant enhancement in serum LH levels detected in rats with autoimmune orchitis suggests the existence of local control mechanisms [13].

Biological context of Orchitis

• Susceptibility to autoimmune orchitis is associated with an immune response (Ir) gene (now designated Orch-1) which was preliminarily shown to reside at or near the H-2D subregion of the major histocompatibility complex in the mouse (H-2) [15].
• Only those inbred and H-2 congenic strains of mice possessing both the H-2d haplotype and the locus for susceptibility to B. pertussis-induced sensitivity to histamine developed autoimmune orchitis [12].
• Partial inhibition of cell-mediated immunity (CMI) by niridazole: effect upon development of autoimmune aspermatogenic orchitis (AIAO) in guinea pigs [16].
• These data suggest that increased Fas expression on the cell surface might be a key event in the pathogenesis of autoimmune orchitis, by inducing a leakage of the blood-tubular barrier as a consequence of Sertoli cell apoptosis [17].
• Our studies utilizing the murine model of experimental allergic orchitis have clearly demonstrated that both classical (class II antigens) and nonclassical major histocompatibility complex-linked immune response genes play a central role in controlling disease susceptibility [18].

Anatomical context of Orchitis

• Linear staining of the basement membrane for IgG and C3 in two cases suggests the development of antibasement membrane orchitis [19].
• The immunological work-up for antibodies in sera or seminal plasma gave normal results for the patients diagnosed with orchitis, as well as the controls [20].
• In conclusion, using a model of autoimmune orchitis our results show that circulating inhibin B levels and inhibin alpha-subunit expression in Sertoli cell cytoplasm closely correlate with the degree of damage of the germinal epithelium [21].
• 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 [22].
• In conclusion, we demonstrated in vivo that MCP-1 is highly expressed in testicular interstitial cells suggesting that this chemokine has an important role in recruiting immune cells to the testis in rats undergoing autoimmune orchitis [23].

Gene context of Orchitis

• Monocyte chemoattractant protein-1 (MCP-1/CCL2) in experimental autoimmune orchitis [23].
• A 2-fold increase in the number of mononuclear cells that express CCR2 was also found in rats with orchitis compared with controls [23].
• Susceptibility to experimental allergic orchitis, which is controlled by the Orch-1 locus, is one example [24].
• Essential pathogenic role for endogenous interferon-gamma (IFN-gamma) during disease onset phase of murine experimental autoimmune orchitis. I. In vivo studies [25].
• Observations on autoimmune orchitis in sterile mice carrying a recessive lethal mutation at the T/t complex exhibiting spontaneous allergic orchitis [26].

References