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兔在/GI.2感染期间的细胞凋亡激活

Apoptosis activation during /GI.2 infection in rabbits.

作者信息

Bębnowska Dominika, Hrynkiewicz Rafał, Wiśniewska Karolina, Żabińska Magdalena, Rintz Estera, Pierzynowska Karolina, Niedźwiedzka-Rystwej Paulina

机构信息

Institute of Biology, University of Szczecin, Szczecin, Poland.

Department of Molecular Biology, Faculty of Biology, University of Gdańsk, Gdańsk, Poland.

出版信息

Front Microbiol. 2024 Jan 25;14:1308018. doi: 10.3389/fmicb.2023.1308018. eCollection 2023.

DOI:10.3389/fmicb.2023.1308018
PMID:38333074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10851742/
Abstract

Rabbit Haemorrhagic Disease (RHD) is a severe disease caused by /GI.1 and GI.2. Immunological processes such as apoptosis are important factors involved in the pathogenesis of Rabbit Haemorrhagic Disease (RHD). The process of programmed cell death has been quite well characterized in infection with GI.1 strains, but apoptosis in infection with GI.2 strains has not been widely studied. This is particularly important as several studies have shown that significant differences in the host immune response are observed during infection with different strains of . In this study, we analyzed the gene expression, protein levels and activity of key apoptotic cell death factors in the spleen, kidney, lung, and heart of rabbits. As a result, we showed that there is a significant increase in and mRNA gene expression ratio in organs of infected animals. Our results show also increased levels of cleaved caspase-3, caspase-6 and PARP. Moreover, significant activity of caspase-3 was also detected. Our results indicate that caspase-3, caspase-6 and genes coding Bcl2 family proteins play a key role in the apoptotic response in /GI.2 infection in organs that are not the target of virus replication.

摘要

兔出血性疾病(RHD)是由/GI.1和GI.2引起的一种严重疾病。诸如细胞凋亡等免疫过程是兔出血性疾病(RHD)发病机制中的重要因素。程序性细胞死亡过程在GI.1毒株感染中已有相当充分的特征描述,但GI.2毒株感染中的细胞凋亡尚未得到广泛研究。这一点尤为重要,因为多项研究表明,在感染不同毒株的过程中观察到宿主免疫反应存在显著差异。在本研究中,我们分析了兔脾脏、肾脏、肺和心脏中关键凋亡细胞死亡因子的基因表达、蛋白质水平和活性。结果表明,感染动物器官中的和mRNA基因表达比率显著增加。我们的结果还显示,裂解的半胱天冬酶-3、半胱天冬酶-6和聚(ADP-核糖)聚合酶(PARP)水平升高。此外,还检测到半胱天冬酶-3的显著活性。我们的结果表明,半胱天冬酶-3、半胱天冬酶-6以及编码Bcl2家族蛋白的基因在非病毒复制靶器官的/GI.2感染的凋亡反应中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/afd0dc6a09fa/fmicb-14-1308018-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/f38e8e073afc/fmicb-14-1308018-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/b657622c728e/fmicb-14-1308018-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/67bea7697605/fmicb-14-1308018-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/3bf3bb934f51/fmicb-14-1308018-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/afd0dc6a09fa/fmicb-14-1308018-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/f38e8e073afc/fmicb-14-1308018-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/b657622c728e/fmicb-14-1308018-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/67bea7697605/fmicb-14-1308018-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/3bf3bb934f51/fmicb-14-1308018-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f364/10851742/afd0dc6a09fa/fmicb-14-1308018-g005.jpg

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