Deng Xueling, Li Shitao, Wu Yuhong, Yao Jiali, Hou Wei, Zheng Jiangyao, Liang Boying, Liang Xiaole, Hu Qiping, Wu Zhanshuai, Tang Zeli
Department of Cell Biology and Genetics, School of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Key Laboratory of Longevity and Aging-related Diseases of Chinese Ministry of Education, Guangxi Medical University, Nanning, China.
Microbiol Spectr. 2025 Feb 4;13(2):e0155024. doi: 10.1128/spectrum.01550-24. Epub 2024 Dec 27.
remains a non-negligible global zoonosis, imposing serious socio-economic burdens in endemic regions. The interplay between gut microbiota and the host transcriptome is crucial for maintaining health; however, the impact of juvenile infection on these factors is still poorly understood. This study aimed to investigate their relationship and potential pathogenic mechanisms. The BALB/c mouse model of early infection with juvenile was constructed. Pathological analyses revealed that juvenile triggered liver inflammation, promoted intestinal villi growth, and augmented goblet cell numbers in the ileum. Additionally, the infection altered the diversity and structure of gut microbiota, particularly affecting beneficial bacteria that produce short-chain fatty acids, such as and , and disrupted the Firmicutes/Bacteroidetes ratio. Gut transcriptome analysis demonstrated an increase in the number of differentially expressed genes (DEGs) as infection progressed. Enriched Gene Ontology items highlighted immune and detoxification-related processes, including immunoglobulin production and xenobiotic metabolic processes. Kyoto Encyclopedia of Genes and Genomes pathway analysis further indicated involvement in circadian rhythm, as well as various detoxification and metabolic-related pathways (e.g., glutathione metabolism and glycolysis/gluconeogenesis). Prominent DEGs associated with these pathways included Igkv12-41, Mcpt2, Arntl, Npas2, Cry1, and Gsta1. Correlation analysis additionally identified as a potential key regulator in the interaction between gut microbiota and transcriptome. This study sheds light on the alterations in gut microbiota and transcriptome in mice following juvenile infection, as well as their correlation, laying a foundation for a better understanding of their interaction during infection.
This study highlighted the impact of juvenile infection on the gut microbiota and transcriptome of BALB/c mice. It induced liver inflammation, promoted intestinal villi growth, and altered goblet cell numbers. The infection also disrupted the diversity and structure of gut microbiota, particularly affecting beneficial bacteria. Transcriptome analysis revealed increased expression of genes related to immune response and detoxification processes. Important pathways affected included circadian rhythm, glutathione metabolism, and glycolysis/gluconeogenesis. Notable genes implicated included Igkv12-41, Mcpt2, Arntl, Npas2, Cry1, and Gsta1. emerged as a potential key regulator in this interaction.
仍是一种不可忽视的全球人畜共患病，在流行地区带来严重的社会经济负担。肠道微生物群与宿主转录组之间的相互作用对于维持健康至关重要；然而，幼年感染对这些因素的影响仍知之甚少。本研究旨在探讨它们之间的关系及潜在致病机制。构建了幼年感染的BALB/c小鼠模型。病理分析显示，幼年感染引发肝脏炎症，促进肠绒毛生长，并增加回肠杯状细胞数量。此外，感染改变了肠道微生物群的多样性和结构，尤其影响产生短链脂肪酸的有益细菌，如和，并破坏了厚壁菌门/拟杆菌门的比例。肠道转录组分析表明，随着感染进展，差异表达基因（DEG）数量增加。富集的基因本体论条目突出了免疫和解毒相关过程，包括免疫球蛋白产生和外源性代谢过程。京都基因与基因组百科全书通路分析进一步表明其参与昼夜节律以及各种解毒和代谢相关通路（如谷胱甘肽代谢和糖酵解/糖异生）。与这些通路相关的显著DEG包括Igkv12 - 41、Mcpt2、Arntl、Npas2、Cry1和Gsta1。相关性分析还确定为肠道微生物群与转录组相互作用中的潜在关键调节因子。本研究揭示了幼年感染后小鼠肠道微生物群和转录组的变化及其相关性，为更好地理解感染期间它们的相互作用奠定了基础。
本研究突出了幼年感染对BALB/c小鼠肠道微生物群和转录组的影响。它诱导肝脏炎症，促进肠绒毛生长，并改变杯状细胞数量。感染还破坏了肠道微生物群的多样性和结构，尤其影响有益细菌。转录组分析显示与免疫反应和解毒过程相关的基因表达增加。受影响的重要通路包括昼夜节律、谷胱甘肽代谢和糖酵解/糖异生。涉及的显著基因包括Igkv12 - 41、Mcpt2、Arntl、Npas2、Cry1和Gsta1。在这种相互作用中成为潜在的关键调节因子。
