Li Jinqiu, Chen Zhonghui, Yan Xingchen, Chen Qizhou, Chen Cirong, Liu Huan, Shen Jianlin
Central Laboratory, Affiliated Hospital of Putian University, Putian University, Putian, Fujian, 351100, China.
Guangdong Academy of Sciences, Guangdong-Hong Kong Joint Laboratory of Modern Surface Engineering Technology, Guangdong Provincial Key Laboratory of Modern Surface Engineering Technology, Guangzhou, Guangdong, 510651, China.
BMC Microbiol. 2025 May 22;25(1):315. doi: 10.1186/s12866-025-04035-y.
The gut microbiota plays a crucial role in host health. Recent study revealed that ubiquitin-specific protease 25 (USP25) deficiency affected colonic immune responses and resistance to certain bacterial infection. This study aimed to investigate the impact of USP25 gene deletion on the gut microbiota of mice, utilizing 16 S rRNA amplicon sequencing and metagenomic sequencing to provide a comprehensive analysis of microbial diversity, composition and functional characteristics.
We collected fecal samples from 10 wild type (WT) C57BL/6J mice and 10 USP25 mice (C57BL/6J-Usp25cyagen) for 16 S rRNA amplicon sequencing. Subsequently, the 6 of the 20 samples underwent further analysis using metagenomic sequencing.
Our results revealed significant differences in the gut microbiota between USP25 knockout (KO) mice and wild-type (WT) controls, with KO mice exhibiting 1,858 unique amplicon sequence variants (ASVs) compared to 1,723 in WT mice. Notably, the KO group displayed a higher tendency for biofilm formation and a greater proportion of gram-negative bacteria, while the WT group demonstrated enhanced stress tolerance and a higher presence of gram-positive bacteria. Functional prediction analyses indicated an increase in antibiotic resistance genes in the KO mice, particularly for tetracycline, cephalosporin, and sulfonamides, suggesting a potential risk for clinical antibiotic treatment efficacy. Moreover, KEGG pathway enrichment analysis revealed significant enrichment for fructose and mannose metabolism, streptomycin biosynthesis in the KO group. Furthermore, an increase in protective microbes alongside a decrease in potential pathogens in the KO microbiota hinted at altered immune responses due to USP25 deletion.
Our findings elucidate the essential role of USP25 in modulating gut microbiota composition and function, providing insights for future therapeutic strategies targeting gut microbiota in disease contexts.
Not applicable.
肠道微生物群在宿主健康中起着至关重要的作用。最近的研究表明，泛素特异性蛋白酶25（USP25）缺陷会影响结肠免疫反应和对某些细菌感染的抵抗力。本研究旨在利用16S rRNA扩增子测序和宏基因组测序对小鼠肠道微生物群进行综合分析，以探讨USP25基因缺失对小鼠肠道微生物群的影响，包括微生物多样性、组成和功能特征。
我们收集了10只野生型（WT）C57BL/6J小鼠和10只USP25小鼠（C57BL/6J-Usp25cyagen）的粪便样本进行16S rRNA扩增子测序。随后，对20个样本中的6个进行宏基因组测序进一步分析。
我们的结果显示，USP25基因敲除（KO）小鼠与野生型（WT）对照的肠道微生物群存在显著差异，KO小鼠表现出1858个独特的扩增子序列变体（ASV），而WT小鼠为1723个。值得注意的是，KO组显示出更高的生物膜形成倾向和更大比例的革兰氏阴性菌，而WT组表现出增强的应激耐受性和更高比例的革兰氏阳性菌。功能预测分析表明，KO小鼠中抗生素抗性基因增加，尤其是对四环素、头孢菌素和磺胺类药物，这表明临床抗生素治疗效果存在潜在风险。此外，KEGG通路富集分析显示，KO组中果糖和甘露糖代谢、链霉素生物合成显著富集。此外，KO微生物群中保护性微生物增加而潜在病原体减少，这暗示由于USP25缺失导致免疫反应改变。
我们的研究结果阐明了USP25在调节肠道微生物群组成和功能中的重要作用，为未来在疾病背景下针对肠道微生物群的治疗策略提供了见解。
不适用。
