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COVID-19 disrupts the blood–testis barrier through the induction of inflammatory cytokines and disruption of junctional proteins
Inflammation Research ( IF 4.8 ) Pub Date : 2021-08-26 , DOI: 10.1007/s00011-021-01497-4
Tahmineh Peirouvi 1 , Abbas Aliaghaei 2 , Bahram Eslami Farsani 3 , Sanaz Ziaeipour 2 , Vahid Ebrahimi 4 , Mehdi Forozesh 5 , Masoud Ghadipasha 5 , Gholam-Reza Mahmoudiasl 6 , Arefeh Aryan 7 , Negin Moghimi 1, 2 , Shabnam Abdi 8 , Amir Raoofi 9 , Mohammadhossein Kargar Godaneh 2 , Mohammad-Amin Abdollahifar 2
Affiliation  

Objective

Junctional proteins are the most important component of the blood-testis barrier and maintaining the integrity of this barrier is essential for spermatogenesis and male fertility. The present study elucidated the effect of SARS-CoV-2 infection on the blood–testis barrier (BTB) in patients who died from severe acute respiratory syndrome coronavirus 2 (COVID-19) complications.

Methods

In this study, lung and testis tissue was collected from autopsies of COVID-19 positive (n = 10) and negative men (n = 10) and was taken for stereology, immunocytochemistry, and RNA extraction.

Results

Evaluation of the lung tissue showed that the SARS-CoV-2 infection caused extensive damage to the lung tissue and also increases inflammation in testicular tissue and destruction of the testicular blood barrier. Autopsied testicular specimens of COVID-19 showed that COVID-19 infection significantly changes the spatial arrangement of testicular cells and notably decreased the number of Sertoli cells. Moreover, the immunohistochemistry results showed a significant reduction in the protein expression of occluding, claudin-11, and connexin-43 in the COVID-19 group. In addition, we also observed a remarkable enhancement in protein expression of CD68 in the testes of the COVID-19 group in comparison with the control group. Furthermore, the result showed that the expression of TNF-α, IL1β, and IL6 was significantly increased in COVID-19 cases as well as the expression of occludin, claudin-11, and connexin-43 was decreased in COVID-19 cases.

Conclusions

Overall, the present study demonstrated that SARS-CoV-2 could induce the up-regulation of the pro-inflammatory cytokine and down-regulation of junctional proteins of the BTB, which can disrupt BTB and ultimately impair spermatogenesis.



中文翻译:


COVID-19 通过诱导炎症细胞因子和破坏连接蛋白来破坏血睾屏障


 客观的


连接蛋白是血睾屏障最重要的组成部分,维持该屏障的完整性对于精子发生和男性生育能力至关重要。本研究阐明了 SARS-CoV-2 感染对死于严重急性呼吸综合征冠状病毒 2 (COVID-19) 并发症的患者血睾屏障 (BTB) 的影响。

 方法


在这项研究中,从 COVID-19 阳性 ( n = 10) 和阴性男性 ( n = 10) 的尸检中收集肺和睾丸组织,并进行体视学、免疫细胞化学和 RNA 提取。

 结果


对肺组织的评估表明,SARS-CoV-2感染对肺组织造成了广泛的损伤,还增加了睾丸组织的炎症和睾丸血屏障的破坏。 COVID-19的尸检睾丸标本表明,COVID-19感染显着改变了睾丸细胞的空间排列,并且显着减少了支持细胞的数量。此外,免疫组化结果显示,COVID-19组中occlusion、claudin-11和connexin-43的蛋白表达显着降低。此外,我们还观察到与对照组相比,COVID-19组睾丸中CD68蛋白表达显着增强。此外,结果显示,COVID-19病例中TNF-α、IL1β和IL6的表达显着升高,而occludin、claudin-11和connexin-43的表达在COVID-19病例中降低。

 结论


总体而言,本研究表明 SARS-CoV-2 可以诱导促炎细胞因子的上调和 BTB 连接蛋白的下调,从而破坏 BTB 并最终损害精子发生。

更新日期:2021-08-26
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