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高致病性猪繁殖与呼吸综合征病毒感染诱导感染仔猪胸腺细胞凋亡和自噬

Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets.

作者信息

Wang Gang, Yu Ying, Tu Yabin, Tong Jie, Liu Yonggang, Zhang Chong, Chang Yafei, Wang Shujie, Jiang Chenggang, Zhou En-Min, Cai Xuehui

机构信息

State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China.

State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China; Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, 712100, PR China.

出版信息

PLoS One. 2015 Jun 5;10(6):e0128292. doi: 10.1371/journal.pone.0128292. eCollection 2015.

Abstract

Previously, we demonstrated that the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) HuN4 strain causes obvious thymic atrophy and thymocytes apoptosis in infected piglets after birth, which is more severe than that induced by classical PRRSV. In this study, we investigated apoptosis and autophagy in the thymus of piglets infected with the HP-PRRSV HuN4 strain, and found that both apoptosis and autophagy occurred in the thymus of piglets infected with HP-PRRSV. In addition to a few virus-infected cells, CD14+ cells, the main autophagic cells in the thymus were thymic epithelial cells. These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets. Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets. Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

摘要

先前,我们证明了高致病性猪繁殖与呼吸综合征病毒(HP-PRRSV)HuN4株在感染仔猪出生后可导致明显的胸腺萎缩和胸腺细胞凋亡,且比经典PRRSV诱导的更为严重。在本研究中,我们调查了感染HP-PRRSV HuN4株的仔猪胸腺中的凋亡和自噬情况,发现感染HP-PRRSV的仔猪胸腺中同时发生了凋亡和自噬。除了少数病毒感染细胞外,胸腺中主要的自噬细胞CD14+细胞是胸腺上皮细胞。这些发现表明,HP-PRRSV可诱导旁观者细胞凋亡,并在感染仔猪的胸腺中诱导感染细胞和旁观者细胞发生自噬。在此,我们首次展示了HP-PRRSV诱导胸腺病变的新数据,并表明凋亡和自噬是参与感染仔猪细胞存活的关键机制以及胸腺萎缩严重程度的决定因素。最后,基于我们目前对PRRSV-宿主相互作用的理解,提出了未来对免疫反应潜在机制的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7977/4457848/3d5716c8c39c/pone.0128292.g001.jpg

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