兔感染引起出血热的动物病毒期间自噬和凋亡标志物的评估。
Evaluation of autophagic and apoptotic markers during infection with animal virus causing hemorrhagic fever in rabbits.
作者信息
Bębnowska Dominika, Rzeszotek Sylwia, Kolasa Agnieszka, Wiśniewska Karolina, Żabińska Magdalena, Szulc Aneta, Cyske Zuzanna, Pierzynowska Karolina, Wilk Aleksandra, Niedźwiedzka-Rystwej Paulina
机构信息
Institute of Biology, University of Szczecin, Szczecin, Poland.
Center for Experimental Immunology and Immunobiology in Infectious Disease and Cancer, University of Szczecin, Szczecin, Poland.
出版信息
Front Microbiol. 2025 Jan 8;15:1517725. doi: 10.3389/fmicb.2024.1517725. eCollection 2024.
INTRODUCTION
/GI.1 and GI.2 cause severe Rabbit Haemorrhagic Disease, and immune processes are among the important pathomechanisms of the disease. Autophagy and apoptosis are two key mechanisms involved in the host antiviral response. Both of these processes have been characterized in infection with GI.1 strains, while data on infection with GI.2 strains still need to be studied. This is particularly important because infection with different strains is associated with a different host immune response profile.
METHODS
In this work, we analyzed the expression of selected genes and proteins involved in autophagic flux in the liver, spleen, kidney and peripheral blood, but also apoptotic cell death in the liver and peripheral blood of rabbits infected with the GI.2 strain.
RESULTS
As a result, we showed that autophagy is strongly activated in the liver, spleen and kidney of infected rabbits, and confirmed the activation of apoptosis in the liver.
DISCUSSION
This study highlights the role of apoptosis and autophagy in the immune response in rabbits infected with Lagovirus europaeus/GI.2.
引言
/GI.1和GI.2会引发严重的兔出血性疾病，免疫过程是该疾病重要的发病机制之一。自噬和凋亡是宿主抗病毒反应涉及的两个关键机制。这两个过程在GI.1毒株感染中均有特征描述，而关于GI.2毒株感染的数据仍有待研究。这一点尤为重要，因为不同毒株感染与不同的宿主免疫反应特征相关。
方法
在本研究中，我们分析了感染GI.2毒株的兔肝脏、脾脏、肾脏和外周血中参与自噬通量的特定基因和蛋白质的表达情况，以及肝脏和外周血中凋亡细胞死亡情况。
结果
结果显示，感染兔肝脏、脾脏和肾脏中的自噬被强烈激活，并证实肝脏中存在凋亡激活。
讨论
本研究强调了凋亡和自噬在感染欧洲兔病毒/GI.2的兔免疫反应中的作用。
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