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Abstract：
Sperm granuloma may develop in the epididymis following vasectomy or chemical insults. Inflammation due to sperm granuloma causes abdominal and scrotal pain. Prolonged and persistent inflammation in the epididymis due to sperm granuloma may lead to infertility. Extravasation of germ cells into the interstitium of epididymis following damage of the epididymal epithelium is one of the primary reasons for sperm granuloma-associated pathology. Since testosterone is vital for the maintenance of epididymal epithelium, we investigated the pathology of sperm granuloma and its relationship with testosterone. Adult rats were treated with a Leydig cell-specific toxicant ethylene dimethane sulfonate (EDS) to eliminate testosterone. At 7 days post-EDS, disrupted epididymal epithelium and sperm granuloma were observed in the caput epididymis. Sperm granuloma and caput were collagen-filled indicating fibrosis. Numerous round apoptotic cells were localized inside the caput lumen and dispersed through the sperm granuloma. Tnp1 (round spermatid marker) was significantly higher in the epididymis of the EDS-treated group compared to controls suggesting the apoptotic cells were round spermatids. Increases in CD68+ macrophages and T cells (CD4 and CD8) support an inflammatory immune infiltration in post-EDS epididymis. However, testosterone replacement following EDS prevented the sperm granuloma-associated pathology. We suggest that the immune response in the sperm granuloma may be due to the increased numbers of apoptotic round spermatids or other testicular tissue components that may be released, in addition to the regression of epididymal epithelium due to testosterone loss. Thus, testosterone replacement prevents EDS-induced sperm granuloma and ameliorates sperm granuloma-associated pathology.
摘要：
输精管结扎或化学损伤后，精子肉芽肿可能在附睾发展。精子肉芽肿引起的炎症引起腹部和阴囊疼痛。由于精子肉芽肿引起的附睾长期和持续的炎症可能导致不孕。附睾上皮损伤后生殖细胞外渗到附睾间质是精子肉芽肿相关病理的主要原因之一。由于睾酮对于维持附睾上皮至关重要，我们调查了精子肉芽肿的病理及其与睾酮的关系。成年大鼠用Leydig细胞特异性毒物乙烯二甲烷磺酸盐（EDS）处理以消除睾丸激素。在EDS后7天，在附睾中观察到附睾上皮破裂和精子肉芽肿。精子肉芽肿和caput是胶原蛋白填充的，表明纤维化。许多圆形凋亡细胞位于头腔内，并分散在精子肉芽肿中。与对照组相比，EDS治疗组的附睾中的Tnp1（圆形精子细胞标记）显着高于对照组，表明凋亡细胞是圆形精子细胞。CD68+巨噬细胞和T细胞(CD4和CD8)的增加支持EDS后附睾的炎性免疫浸润。然而,EDS后睾酮替代可预防精子肉芽肿相关病理。我们认为精子肉芽肿中的免疫反应可能是由于凋亡的圆形精子细胞或其他可能释放的睾丸组织成分的数量增加，除了由于睾酮损失引起的附睾上皮消退。因此，睾酮替代可预防EDS诱导的精子肉芽肿并改善精子肉芽肿相关病理。
