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感染对家禽脾脏免疫机制影响的比较组学分析

Comparative omics analysis of the impact of infection on the immune mechanisms of poultry spleen.

作者信息

Zhong Lemiao, Wu Chunlin, Liao Lvyan, Li Jian, Wu Yijian

机构信息

College of Animal Science, Fujian Agriculture and Forestry University, Fuzhou, People's Republic of China.

Fujian Provincial Department of Education, Key Laboratory of Integrated Traditional Chinese and Western Veterinary Medicine and Animal Health, Fuzhou, China.

出版信息

Virulence. 2025 Dec;16(1):2507197. doi: 10.1080/21505594.2025.2507197. Epub 2025 Jun 9.

DOI:10.1080/21505594.2025.2507197
PMID:40485328
Abstract

(MS) infection can cause severe inflammatory responses in avian species, evading immune recognition, leading to chronic infection and immune dysfunction. Although the pathogenic mechanisms and immune evasion strategies of MS have not been fully elucidated, the crucial role of the spleen in immune responses cannot be overlooked. Building on preliminary findings related to the tissue damage and inflammatory responses in chicken spleens caused by MS infection, this study further utilizes transcriptomic and proteomic technologies to thoroughly investigate the comprehensive effects of MS infection on the chicken spleen. We detected 946 differentially expressed genes (DEGs) and 305 differentially expressed proteins (DEPs) during MS infection, including 771 up-regulated and 175 down-regulated DEGs, along with 145 up-regulated and 160 down-regulated DEPs. Gene Ontology (GO) analysis indicated that the DEGs/DEPs are enriched in processes related to immune activation, antioxidation/cell apoptosis, inflammation, and endoplasmic reticulum protein processing. KEGG pathway enrichment analysis revealed immune-related pathways closely associated with MS infection, particularly in endoplasmic reticulum protein processing, cytokine-cytokine receptor interaction, and the myosin light chain kinase (MAPK) signalling pathway. Suggesting that the activation and interaction of these pathways may play a critical role in the immune response during MS infection. Overall, this study, for the first time, employs RNA-Seq and TMT quantitative proteomics to comprehensively analyse the interaction mechanisms between MS and chicken spleen, enhancing our understanding of the complexity of the immune mechanisms induced by MS. This provides valuable insights for future research and intervention strategies targeting MS infection.

摘要

(鸡败血支原体)感染可在禽类中引发严重的炎症反应,逃避免疫识别,导致慢性感染和免疫功能障碍。尽管鸡败血支原体的致病机制和免疫逃避策略尚未完全阐明,但脾脏在免疫反应中的关键作用不容忽视。基于鸡败血支原体感染引起的鸡脾脏组织损伤和炎症反应的初步研究结果,本研究进一步利用转录组学和蛋白质组学技术,全面探究鸡败血支原体感染对鸡脾脏的综合影响。我们在鸡败血支原体感染期间检测到946个差异表达基因(DEGs)和305个差异表达蛋白(DEPs),其中包括771个上调和175个下调的DEGs,以及145个上调和160个下调的DEPs。基因本体(GO)分析表明,这些DEGs/DEPs在与免疫激活、抗氧化/细胞凋亡、炎症和内质网蛋白加工相关的过程中富集。京都基因与基因组百科全书(KEGG)通路富集分析揭示了与鸡败血支原体感染密切相关的免疫相关通路,特别是在内质网蛋白加工、细胞因子-细胞因子受体相互作用和丝裂原活化蛋白激酶(MAPK)信号通路中。这表明这些通路的激活和相互作用可能在鸡败血支原体感染期间的免疫反应中起关键作用。总体而言,本研究首次采用RNA测序和TMT定量蛋白质组学全面分析鸡败血支原体与鸡脾脏之间的相互作用机制,加深了我们对鸡败血支原体诱导的免疫机制复杂性的理解。这为未来针对鸡败血支原体感染的研究和干预策略提供了有价值的见解。

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本文引用的文献

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MicroRNA-126-3P targets PIK3R2 to ameliorate autophagy and apoptosis of cortex in hypoxia-reoxygenation treated neonatal rats.微小 RNA-126-3P 通过靶向 PIK3R2 改善缺氧复氧处理新生大鼠皮质细胞的自噬和凋亡。
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induce spleen tissue damage and inflammatory response of chicken through oxidative stress and apoptosis.
通过氧化应激和细胞凋亡诱导鸡脾脏组织损伤和炎症反应。
Virulence. 2023 Nov 14:2283895. doi: 10.1080/21505594.2023.2283895.
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Molecular basis for potent B cell responses to antigen displayed on particles of viral size.病毒样颗粒表面展示抗原诱导强烈 B 细胞反应的分子基础。
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Extracellular Vesicles Released from Macrophages Infected with Stimulate Proinflammatory Response via the TLR2-NF-κB/JNK Signaling Pathway.巨噬细胞来源的细胞外囊泡通过 TLR2-NF-κB/JNK 信号通路被 刺激后促进促炎反应。
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Pathogen-selective killing by guanylate-binding proteins as a molecular mechanism leading to inflammasome signaling.鸟苷酸结合蛋白的病原体选择性杀伤作用作为导致炎症小体信号转导的分子机制。
Nat Commun. 2022 Jul 29;13(1):4395. doi: 10.1038/s41467-022-32127-0.
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Peucedanum praeruptorum Dunn polysaccharides regulate macrophage inflammatory response through TLR2/TLR4-mediated MAPK and NF-κB pathways.前胡多糖通过 TLR2/TLR4 介导的 MAPK 和 NF-κB 通路调节巨噬细胞炎症反应。
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