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急性低氧应激介导轴以促进在中的感染。 (你提供的原文似乎不太完整,部分内容缺失,导致翻译出来的句子不太通顺准确。)

Acute hypoxia stress mediates axis to facilitate the infection of in .

作者信息

He Honghui, Huang Shaoqing, Geng Ningze, Weng Shaoping, He Jianguo, Li Chaozheng

机构信息

State Key Laboratory of Biocontrol/School of Marine Sciences, Sun Yat-sen University, Guangzhou, China.

Southern Marine Sciences and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, China.

出版信息

Front Immunol. 2024 Nov 27;15:1476309. doi: 10.3389/fimmu.2024.1476309. eCollection 2024.

Abstract

INTRODUCTION

Hypoxia stress renders aquatic animals more susceptible to bacterial disease, yet the underlying mechanism remains elusive.

METHODS

We conducted an acute hypoxia stress experiment to investigate the impact of stress on the immune response of via transcriptome analysis, RT-qPCR and Western blot.

RESULTS

Our results showed that acute hypoxia stress disrupted the tissue architecture, and significantly changed the gene expression profiles in the hepatopancreas of shrimp. More importantly, acute hypoxia stress significantly changed the expression levels of immune-related genes. , , , , and were significantly down-regulated, but , , , , and were significantly up-regulated. We further demonstrated that acute hypoxia activated via to enhance expression level of , and then inhibited the phosphorylation of Dorsal and its nuclear translocation, thereby suppressing antibacterial immunity. Subsequently, the challenge experiment following stress revealed that exposure to acute hypoxia stress amplified the infectivity and lethality of to shrimp. The mechanism of axis provided an explanation for this phenomenon.

DISCUSSION

This study offered new insights into interactions among environmental hypoxia stress, host immunity and pathogens, thereby providing practical guidelines for optimizing shrimp culture practices.

摘要

引言

缺氧应激使水生动物更容易感染细菌性疾病,但其潜在机制仍不清楚。

方法

我们进行了一项急性缺氧应激实验,通过转录组分析、RT-qPCR和蛋白质免疫印迹法研究应激对虾免疫反应的影响。

结果

我们的结果表明,急性缺氧应激破坏了组织结构,并显著改变了虾肝胰腺中的基因表达谱。更重要的是,急性缺氧应激显著改变了免疫相关基因的表达水平。、、、、和显著下调,但、、、、和显著上调。我们进一步证明,急性缺氧通过激活来增强的表达水平,然后抑制Dorsal的磷酸化及其核转位,从而抑制抗菌免疫。随后,应激后的攻毒实验表明,暴露于急性缺氧应激会增强对虾的感染力和致死率。轴的机制为这一现象提供了解释。

讨论

本研究为环境缺氧应激、宿主免疫和病原体之间的相互作用提供了新的见解,从而为优化对虾养殖实践提供了实用指南。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/014b/11632965/aec57e88891b/fimmu-15-1476309-g001.jpg

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