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A型致鹿肠炎中的氧化应激与肠道转录组变化

Oxidative Stress and Intestinal Transcriptome Changes in Type A-Caused Enteritis in Deer.

作者信息

Wang Meihui, Guo Qingyun, Zhong Zhenyu, Zhang Qingxun, Shan Yunfang, Cheng Zhibin, Wang Xiao, Meng Yuping, Dong Yulan, Bai Jiade

机构信息

Laboratory of Veterinary Anatomy, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.

Beijing Milu Ecological Research Center, Beijing 100076, China.

出版信息

Genes (Basel). 2025 Aug 11;16(8):949. doi: 10.3390/genes16080949.


DOI:10.3390/genes16080949
PMID:40869997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12386127/
Abstract

BACKGROUND: () type A is a major cause of enteritis in farmed and wild deer populations, leading to significant economic losses in the deer industry. This bacterium produces toxins that damage the intestine. METHODS: In this study, we performed transcriptome analysis by establishing an intestinal circulation model of the intestines of fallow deer () inoculated with type A versus those not inoculated with type A. In a further step, we determined the protein content of immunoinflammation-related molecules by ELISA and the antioxidant capacity of the intestine to investigate the molecular mechanisms of type A-induced enteritis. RESULTS: Transcriptome analysis revealed significant enrichment of pathways related to the haematopoietic system, oxidative stress, the immune system and intestinal tight junctions. Additionally, α-toxin enters the intestine and may be recognized by TLR6, activating the immune system, increasing the secretion of various cytokines and inflammasome components, inducing oxidative stress and damaging the intestine. CONCLUSIONS: This study provides a comprehensive transcriptomic basis for understanding the selective differential expression of genes in deer enteritis induced by type A and provides a broader guide for finding therapeutic approaches to deer enteritis.

摘要

背景:A型(细菌名称未给出)是养殖鹿和野生鹿群肠炎的主要病因,给养鹿业造成重大经济损失。这种细菌产生的毒素会损害肠道。 方法:在本研究中,我们通过建立梅花鹿肠道循环模型进行转录组分析,该模型分为接种A型(细菌名称未给出)的肠道和未接种A型(细菌名称未给出)的肠道。进一步地,我们通过酶联免疫吸附测定法确定免疫炎症相关分子的蛋白质含量,并检测肠道的抗氧化能力,以研究A型(细菌名称未给出)诱导肠炎的分子机制。 结果:转录组分析显示与造血系统、氧化应激、免疫系统和肠道紧密连接相关的通路有显著富集。此外,α毒素进入肠道,可能被Toll样受体6(TLR6)识别,激活免疫系统,增加各种细胞因子和炎性小体成分的分泌,诱导氧化应激并损害肠道。 结论:本研究为理解A型(细菌名称未给出)诱导的鹿肠炎中基因的选择性差异表达提供了全面的转录组学基础,并为寻找鹿肠炎的治疗方法提供了更广泛的指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/2ddcdf93d7dc/genes-16-00949-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/fb145a869919/genes-16-00949-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/82bc994daeb2/genes-16-00949-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/4975089d8ce2/genes-16-00949-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/88b1d681b4dd/genes-16-00949-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/6fda1ec436ea/genes-16-00949-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/439b33aa520d/genes-16-00949-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/2ddcdf93d7dc/genes-16-00949-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/fb145a869919/genes-16-00949-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/82bc994daeb2/genes-16-00949-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/4975089d8ce2/genes-16-00949-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/88b1d681b4dd/genes-16-00949-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/6fda1ec436ea/genes-16-00949-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/439b33aa520d/genes-16-00949-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d0/12386127/2ddcdf93d7dc/genes-16-00949-g007.jpg

相似文献

[1]
Oxidative Stress and Intestinal Transcriptome Changes in Type A-Caused Enteritis in Deer.

Genes (Basel). 2025-8-11

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[8]
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本文引用的文献

[1]
Disruption of Claudin-Made Tight Junction Barriers by Enterotoxin: Insights from Structural Biology.

Cells. 2022-3-5

[2]
The Interleukins Orchestrate Mucosal Immune Responses to Infection in the Intestine.

Cells. 2021-12-10

[3]
Lactobacillus acidophilus PIN7 paraprobiotic supplementation ameliorates DSS-induced colitis through anti-inflammatory and immune regulatory effects.

J Appl Microbiol. 2022-4

[4]
Reviewing the importance of TLR-NLRP3-pyroptosis pathway and mechanism of experimental NLRP3 inflammasome inhibitors.

Scand J Immunol. 2022-2

[5]
Bioengineering CXCR4-overexpressing cell membrane functionalized ROS-responsive nanotherapeutics for targeting cerebral ischemia-reperfusion injury.

Theranostics. 2021

[6]
Resveratrol protects intestinal integrity, alleviates intestinal inflammation and oxidative stress by modulating AhR/Nrf2 pathways in weaned piglets challenged with diquat.

Int Immunopharmacol. 2021-10

[7]
CD36 Signaling in Diabetic Cardiomyopathy.

Aging Dis. 2021-6-1

[8]
Research Progress on Oxidative Stress and Its Nutritional Regulation Strategies in Pigs.

Animals (Basel). 2021-5-13

[9]
Prevalence, Genotypic and Phenotypic Characterization and Antibiotic Resistance Profile of Type A and D Isolated from Feces of Sheep () and Goats () in Punjab, Pakistan.

Toxins (Basel). 2020-10-14

[10]
Clostridium perfringens phospholipase C impairs innate immune response by inducing integrated stress response and mitochondrial-induced epigenetic modifications.

Cell Signal. 2020-11

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