Liu Meng-Chuan, Shu Yu-An, Wang Yu-Chin, Tseng Hsiu-Ying, Li Meng-Jia, Yu Yu-Ting, Cheng Hsiu-Chi, Tsai Pei-Jane, Yang Yao-Jong
Department of Pediatrics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Department of Medical Laboratory Science and Biotechnology and Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan.
Mediators Inflamm. 2025 Mar 10;2025:7280675. doi: 10.1155/mi/7280675. eCollection 2025.
Reduction of abundance is related to inflammatory bowel diseases (IBDs), and supplement of it exists protective effects. This study aimed to establish a -colonized mouse model and investigate that the presence of in the gut can ameliorate the severity of dextran sulfate sodium (DSS)-induced colitis. A (ATCC 27768) strain was maintained on the PS-BHI agar plates and manipulated in a strictly anaerobic chamber. A -colonized C57BL/6 mice model was tested by a rectal enema with 1 × 10 bacteria/day for 3 days. The 5% DSS was added to drinking water for 3 days to induce colitis and diarrhea in experimental mice. The clinical, cytological, and histological severities were compared between groups. The -colonized mice model was successfully established via rectal enema with the property of transfer to offspring. DSS treatment altered gut microbiota and significantly attenuated the abundance of in colonized mice. Mice with colonization had significantly improved weight loss, anal bleeding, stool consistency, cecum weight, colon length, and serum amyloid A (SAA) level than those without after DSS treatment. Furthermore, the -colonized mice significantly reduced the transcription levels of TNF-α, INF-γ and IL-18, and epithelial damage and PMN infiltration in the lamina propria and had better preservation of goblet cells than the control group. We have successfully established a mouse model colonized with via rectal enema administration and showed colonization of in the gut has a protective effect against DSS-induced colitis.
[某种物质]丰度的降低与炎症性肠病(IBDs)相关,补充该物质具有保护作用。本研究旨在建立[某种物质]定殖的小鼠模型,并研究肠道中[某种物质]的存在是否可改善葡聚糖硫酸钠(DSS)诱导的结肠炎的严重程度。[某种物质](ATCC 27768)菌株在PS - BHI琼脂平板上培养,并在严格厌氧箱中操作。通过每天直肠灌注1×10⁸个细菌,持续3天来构建[某种物质]定殖的C57BL/6小鼠模型。将5%的DSS添加到饮用水中3天,以诱导实验小鼠发生结肠炎和腹泻。比较各组之间的临床、细胞学和组织学严重程度。通过直肠灌注成功建立了[某种物质]定殖的小鼠模型,且具有传递给后代的特性。DSS处理改变了肠道微生物群,并显著降低了定殖小鼠中[某种物质]的丰度。与未定殖的小鼠相比,定殖[某种物质]的小鼠在DSS处理后体重减轻、肛门出血、粪便稠度、盲肠重量、结肠长度和血清淀粉样蛋白A(SAA)水平均有显著改善。此外,定殖[某种物质]的小鼠显著降低了TNF-α、INF-γ和IL-18的转录水平,减少了固有层上皮损伤和PMN浸润,杯状细胞的保存情况也优于对照组。我们通过直肠灌注给药成功建立了定殖[某种物质]的小鼠模型,并表明肠道中[某种物质]的定殖对DSS诱导的结肠炎具有保护作用。