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鉴定感染猪繁殖与呼吸综合征病毒强毒株/弱毒株的猪肺泡巨噬细胞中差异表达的蛋白质。

Identification of differentially expressed proteins in porcine alveolar macrophages infected with virulent/attenuated strains of porcine reproductive and respiratory syndrome virus.

作者信息

Zhou Yan-Jun, Zhu Jian-Ping, Zhou Tao, Cheng Qun, Yu Ling-Xue, Wang Ya-Xin, Yang Shen, Jiang Yi-Feng, Tong Wu, Gao Fei, Yu Hai, Li Guo-Xin, Tong Guang-Zhi

机构信息

Division of Swine Infectious Diseases, Shanghai Veterinary Research Institute, CAAS, Shanghai, China.

Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.

出版信息

PLoS One. 2014 Jan 21;9(1):e85767. doi: 10.1371/journal.pone.0085767. eCollection 2014.

Abstract

The highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) is still a serious threat to the swine industry. However, the pathogenic mechanism of HP-PRRSV remains unclear. We infected host porcine alveolar macrophages (PAMs) with the virulent HuN4 strain and the attenuated HuN4-F112 strain and then utilized fluorescent two-dimensional difference gel electrophoresis (2D-DIGE) to screen for intracellular proteins that were differentially expressed in host cells infected with the two strains. There were 153 proteins with significant different expression (P<0.01) observed, 42 of which were subjected to mass spectrometry, and 24 proteins were identified. PAM cells infected with the virulent strain showed upregulated expression of pyruvate kinase M2 (PKM2), heat shock protein beta-1 (HSPB1), and proteasome subunit alpha type 6 (PSMA6), which were downregulated in cells infected with the attenuated strain. The upregulation of PKM2 provides sufficient energy for viral replication, and the upregulation of HSPB1 inhibits host cell apoptosis and therefore facilitates mass replication of the virulent strain, while the upregulation of PSMA6 facilitates the evasion of immune surveillance by the virus. Studying on those molecules mentioned above may be able to help us to understand some unrevealed details of HP-PRRSV infection, and then help us to decrease its threat to the swine industry in the future.

摘要

高致病性猪繁殖与呼吸综合征病毒(HP-PRRSV)仍然是养猪业的严重威胁。然而,HP-PRRSV的致病机制仍不清楚。我们用强毒株HuN4和弱毒株HuN4-F112感染宿主猪肺泡巨噬细胞(PAMs),然后利用荧光二维差异凝胶电泳(2D-DIGE)筛选在这两种毒株感染的宿主细胞中差异表达的细胞内蛋白质。观察到153种蛋白质有显著差异表达(P<0.01),其中42种进行了质谱分析,鉴定出24种蛋白质。感染强毒株的PAM细胞中丙酮酸激酶M2(PKM2)、热休克蛋白β-1(HSPB1)和蛋白酶体亚基α6型(PSMA6)的表达上调,而在感染弱毒株的细胞中这些蛋白表达下调。PKM2的上调为病毒复制提供了足够的能量,HSPB1的上调抑制宿主细胞凋亡,从而促进强毒株的大量复制,而PSMA6的上调则促进病毒逃避免疫监视。对上述分子的研究可能有助于我们了解HP-PRRSV感染一些未揭示的细节,进而帮助我们在未来降低其对养猪业的威胁。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8af1/3897507/d3c7f0d42fca/pone.0085767.g001.jpg

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