严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 病毒引起了 2019 年冠状病毒病大流行，男性死亡人数高于女性。附睾分为头、体、尾，表现出区域特异性免疫。 K18-hACE2 小鼠表达人类血管紧张素转换酶 2 (hACE2)，这是一种允许 SARS-CoV-2 感染的受体。然而，使用这种转基因小鼠来评估这种病毒感染对附睾的影响的研究尚未进行。我们评估了SARS-CoV-2感染的K18-hACE2小鼠附睾中hACE2的表达，并评估了附睾免疫反应，重点关注 F4/80 单核吞噬细胞和肿瘤坏死因子-α 表达。在感染小鼠的附睾切片中进行以下分析：上皮高度和导管直径、双折射胶原、末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记、免疫反应用于检测 hACE2、spike、FGF、V-ATPase、F4/80、肿瘤坏死因子-α 和 iNOS。在电子显微镜下鉴定出病毒颗粒。还通过实时定量聚合酶链式反应评估了hACE2、Rigi、Tgfb1和Tnfa的表达。所有附睾区域均表达hACE2，并且在感染小鼠的所有附睾区域中hACE2均增加。然而，该地区似乎是感染最严重的地区。尽管如此，头部区域显示出最小的变化，而尾部显示出与 iNOS 免疫表达增加相关的显着上皮变化。 F4/80单核吞噬细胞面积在基质和上皮中均显着增加。除了上皮和基质单核吞噬细胞外，还在透明细胞中检测到肿瘤坏死因子-α，其细胞质显示这种细胞因子在感染动物中显着增加。K18-hACE2 小鼠是评估肿瘤坏死因子-α 影响的有用模型。附睾中的 SARS-CoV-2 感染。感染诱导 hACE2 上调，有利于附睾的毒力。附睾区域对感染的反应不同，F4/80单核吞噬细胞的激活与透明细胞中肿瘤坏死因子-α免疫标记增加相关，表明透明细胞/单核吞噬细胞免疫调节机制在附睾对SARS-CoV免疫反应中的作用-2 感染。© 2024 美国男科学会和欧洲男科学会。

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus caused the coronavirus disease 2019 pandemic, and the prevalence of deaths among men is higher than among women. The epididymis, divided into caput, corpus, and cauda, shows a region-specific immunity. The K18-hACE2 mouse expresses human angiotensin-converting enzyme 2 (hACE2), the receptor that allows SARS-CoV-2 infection. However, studies using this transgenic mouse to evaluate the impact of this viral infection in epididymis have not yet been performed.We evaluated the expression of hACE2 in the epididymis of SARS-CoV-2-infected K18-hACE2 mice, and assessed the epididymal immune response, focusing on F4/80+ mononuclear phagocytes and tumor necrosis factor-alpha expression.The following analyses were performed in the epididymal sections of infected mice: epithelial height and duct diameter, birefringent collagen, Terminal deoxynucleotidyl Transferase-mediated dUTP Nick End Labelling, immunoreactions for detection of hACE2, spike, FGF, V-ATPase, F4/80, tumor necrosis factor-alpha, and iNOS. Viral particles were identified under electron microscopy. hACE2, Rigi, Tgfb1 and Tnfa expression were also evaluated by real-time quantitative polymerase chain reaction.All epididymal regions expressed hACE2, which increased in all epididymal regions in the infected mice. However, the caput appeared to be the most infected region. Despite this, the caput region showed minimal changes while the cauda showed significant epithelial changes associated with increased iNOS immunoexpression. The F4/80+ mononuclear phagocyte area increased significantly in both stroma and epithelium. In addition to the epithelial and stromal mononuclear phagocytes, tumor necrosis factor-alpha was also detected in clear cells, whose cytoplasm showed a significant increase of this cytokine in the infected animals.The K18-hACE2 mouse is a useful model for evaluating the impact of SARS-CoV-2 infection in the epididymis. The infection induced hACE2 upregulation, favoring the virulence in the epididymis. The epididymal regions responded differentially to infection, and the activation of F4/80+ mononuclear phagocytes associated with the increased tumor necrosis factor-alpha immunolabeling in clear cells indicates a role of clear cells/mononuclear phagocytes immunoregulatory mechanisms in the epididymal immune response to SARS-CoV-2 infection.© 2024 American Society of Andrology and European Academy of Andrology.