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鸡盲肠对肠炎沙门氏菌感染反应的时间转录组分析

Temporal transcriptome profiling in the response to Salmonella enterica serovar enteritidis infection in chicken cecum.

作者信息

Peng Yanan, Li Huilong, Yang Jingchao, Yang Xiaohua, Miao Xiuxiu, Fan Xinzhong, Liu Liying, Li Xianyao

机构信息

Shandong Provincial Key Laboratory for Livestock Germplasm Innovation Utilization, College of Animal Science and Technology, Shandong Agricultural University, Tai'an 271018 China.

Shandong Animal Husbandry General Station, Jinan 250010, China.

出版信息

Poult Sci. 2025 Feb;104(2):104773. doi: 10.1016/j.psj.2025.104773. Epub 2025 Jan 4.

DOI:10.1016/j.psj.2025.104773
PMID:39813862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11782854/
Abstract

Salmonella enterica serovar Enteritidis (S. Enteritidis) is a common zoonotic pathogen that not only causes gastroenteritis or death of livestock and poultry but also poses a serious threat to human health, causing severe economic losses to the poultry industry and society. Herein, RNA-sequencing (RNA-seq) was used to analyze the transcriptome variation of chicken cecum at four different time points (1, 3, 7, and 14 days) following S. Enteritidis infection. There were 529, 1477, 476, and 432 differentially expressed genes (DEGs) in the cecum at four different days post-infection (dpi), respectively. The DEGs were significantly enriched in various immune-related pathways on 3 dpi and 7 dpi, such as cytokine-cytokine-receptor interaction and Toll-like receptor signaling pathway. DEGs were significantly enriched in several metabolic pathways on 14 dpi. Gene ontology (GO) enrichment of DEGs showed that up-regulated genes were significantly enriched in immune-related terms on 3 and 7 dpi. On 14 dpi, up-regulated genes were mainly enriched in the signaling-related terms, while the down-regulated genes were primarily enriched in the metabolic-related terms. Based on weighted gene co-expression network analysis (WGCNA), the key modules related to energy, non-coding processes, immunity, and development-related functions were identified at 1, 3, 7, and 14 dpi, respectively, and 5, 8, 6, and 5 hub genes were screened out, respectively. This study demonstrated that the chicken cecal transcriptome regulation responding to S. Enteritidis infection is time-dependent. The regulation of S. Enteritidis infection in chickens is coordinated by multiple systems, mainly involving immunity, metabolism, and signal transduction. Both 3 and 7 dpi are key time points for immune response. As the infection progresses, metabolism-related pathways were increasingly identified. This change reflects the dynamic adjustment between immune response and metabolism in Jining Bairi chickens following S. Enteritidis infection. These results suggested that starting from 3 dpi, the chickens gradually transition from an immune response triggered by S. Enteritidis infection to a state where they adapt to the infection by modulating their metabolism.

摘要

肠炎沙门氏菌肠炎血清型(肠炎沙门氏菌)是一种常见的人畜共患病原体,不仅会导致畜禽肠胃炎或死亡,还对人类健康构成严重威胁,给家禽业和社会造成严重经济损失。在此,利用RNA测序(RNA-seq)分析肠炎沙门氏菌感染后四个不同时间点(1、3、7和14天)鸡盲肠的转录组变化。感染后不同天数(dpi)时,盲肠中分别有529、1477、476和432个差异表达基因(DEG)。在感染后3 dpi和7 dpi时,DEG在各种免疫相关途径中显著富集,如细胞因子-细胞因子受体相互作用和Toll样受体信号通路。在感染后14 dpi时,DEG在几个代谢途径中显著富集。DEG的基因本体(GO)富集分析表明,在感染后3和7 dpi时,上调基因在免疫相关术语中显著富集。在感染后14 dpi时,上调基因主要富集在信号相关术语中,而下调基因主要富集在代谢相关术语中。基于加权基因共表达网络分析(WGCNA),分别在感染后1、3、7和14 dpi时鉴定出与能量、非编码过程、免疫和发育相关功能相关的关键模块,并分别筛选出5、8、6和5个枢纽基因。本研究表明,鸡盲肠转录组对肠炎沙门氏菌感染的调节具有时间依赖性。肠炎沙门氏菌感染鸡的调节由多个系统协调,主要涉及免疫、代谢和信号转导。感染后3 dpi和7 dpi都是免疫反应的关键时间点。随着感染的进展,越来越多地发现与代谢相关的途径。这种变化反映了济宁百日鸡在肠炎沙门氏菌感染后免疫反应和代谢之间的动态调整。这些结果表明,从感染后3 dpi开始,鸡逐渐从肠炎沙门氏菌感染引发的免疫反应状态转变为通过调节代谢来适应感染的状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/1b8e01506c85/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/8f4bd9065953/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/35ed66261ee2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/256abbef776a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/7b087da8a47c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/f9fc136c0788/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/21dd5b99145f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/1b8e01506c85/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/8f4bd9065953/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/35ed66261ee2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/256abbef776a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/7b087da8a47c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/f9fc136c0788/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/21dd5b99145f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8917/11782854/1b8e01506c85/gr7.jpg

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