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全身炎症负荷导致甲型H1N1流感病毒感染小鼠肝脏损伤。

Systemic Inflammatory Burden Causes Liver Injury in H1N1-Infected Mice.

作者信息

Wang Junbin, Huang Qing, Yang Yun, Tang Cong, Yu Wenhai, Zhou Yanan, Wu Daoju, Li Bai, Yang Hao, Wang Haixuan, Ma Lei, Lu Shuaiyao

机构信息

Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Kunming 650031, China.

State Key Laboratory of Respiratory Health and Multimorbidity, Beijing 100005, China.

出版信息

Viruses. 2025 Aug 18;17(8):1132. doi: 10.3390/v17081132.

DOI:10.3390/v17081132
PMID:40872846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12390729/
Abstract

Clinical evidence has associated H1N1 influenza with liver impairment, yet the underlying mechanisms remain poorly understood. Here, we investigated H1N1-induced liver damage and its potential mechanisms using a BALB/c mouse infection model. Pathological examination and serum aspartate transaminase (AST) and alanine transaminase (ALT) were assessed. Messenger ribonucleic acid-sequence was used to analyze the transcriptomic changes in tissues. Multiple inflammatory cytokines in tissues and inflammatory cells in the blood were detected on the fifth day post-infection. Our results showed that H1N1 infection caused significant liver pathology and elevated serum AST/ALT levels. Transcriptomic analysis revealed significant alterations in liver gene expression profiles following H1N1 infection, particularly in genes associated with inflammatory responses, including those involved in monocyte adhesion/activation and neutrophil/macrophage infiltration. Marked increases in inflammatory mediators were observed in lungs, serum, and liver, accompanied by systemic changes in circulating inflammatory cells, indicating H1N1 triggered a robust systemic inflammatory response. These findings suggest that H1N1-induced liver damage may be associated with the systemic inflammatory response induced by H1N1 and changes in liver gene regulation.

摘要

临床证据表明甲型H1N1流感与肝损伤有关,但其潜在机制仍知之甚少。在此,我们使用BALB/c小鼠感染模型研究了甲型H1N1流感病毒诱导的肝损伤及其潜在机制。评估了病理检查以及血清天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)。采用信使核糖核酸测序分析组织中的转录组变化。在感染后第5天检测组织中的多种炎性细胞因子和血液中的炎性细胞。我们的结果表明,甲型H1N1流感病毒感染导致明显的肝脏病理变化以及血清AST/ALT水平升高。转录组分析显示,甲型H1N1流感病毒感染后肝脏基因表达谱发生显著改变,尤其是与炎症反应相关的基因,包括参与单核细胞黏附/激活以及中性粒细胞/巨噬细胞浸润的基因。在肺、血清和肝脏中观察到炎性介质显著增加,同时循环炎性细胞出现全身性变化,表明甲型H1N1流感病毒引发了强烈的全身炎症反应。这些发现提示,甲型H1N1流感病毒诱导的肝损伤可能与甲型H1N1流感病毒诱导的全身炎症反应以及肝脏基因调控变化有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/2fecf8224726/viruses-17-01132-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/c43e8af0cdcd/viruses-17-01132-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/f4860490073b/viruses-17-01132-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/5e7a94f5dfcd/viruses-17-01132-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/12e695ffab07/viruses-17-01132-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/5bacf26bec27/viruses-17-01132-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/2fecf8224726/viruses-17-01132-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/c43e8af0cdcd/viruses-17-01132-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/f4860490073b/viruses-17-01132-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/5e7a94f5dfcd/viruses-17-01132-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/12e695ffab07/viruses-17-01132-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/5bacf26bec27/viruses-17-01132-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ddd/12390729/2fecf8224726/viruses-17-01132-g006.jpg

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