Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Toxikon Corporation, Bedford, MA, USA.
Methods Mol Biol. 2021;2291:353-364. doi: 10.1007/978-1-0716-1339-9_17.
Previous methods of infecting mice with Shiga toxin-producing E. coli (STEC) required suppression of host immune function or ablation of the gut microbiota to induce susceptibility to gastrointestinal colonization. Consequently, many pathogen-host interactions occurring in immunocompetent hosts during STEC infection and Shiga toxicosis have remained unclear. The following protocol describes the use of dextran sulfate sodium (DSS) to induce a mild colitis in immunocompetent conventional C57BL/6 mice to facilitate susceptibility to STEC infection by oral gavage. STEC colonization in infected mice was confirmed by recovery of live STEC via fecal cultures and quantified via quantitative polymerase chain reaction of fecal DNA for the STEC-specific gene eae. DSS colitis is well established, broadly reproducible, and does not require specialized equipment or high levels of technical proficiency to be a useful method of inducing susceptibility to gastrointestinal STEC colonization. The DSS + STEC mouse model provides a novel and useful tool for the exploration of local STEC-host interactions in the gut environment and the pathogenesis of Shiga toxicosis.
先前感染产志贺毒素大肠杆菌（STEC）的小鼠的方法需要抑制宿主的免疫功能或清除肠道微生物群，以诱导对胃肠道定植的敏感性。因此，许多在免疫功能正常的宿主中发生的病原体-宿主相互作用在 STEC 感染和志贺毒素中毒期间仍然不清楚。本方案描述了使用葡聚糖硫酸钠（DSS）在免疫功能正常的常规 C57BL/6 小鼠中诱导轻度结肠炎，以促进通过口服灌胃感染 STEC。通过粪便培养回收活 STEC 来确认感染小鼠中的 STEC 定植，并通过粪便 DNA 的定量聚合酶链反应对 STEC 特异性基因 eae 进行定量。DSS 结肠炎已经得到很好的证实，广泛可复制，并且不需要专门的设备或高水平的技术熟练程度，是诱导胃肠道 STEC 定植敏感性的有用方法。DSS+STEC 小鼠模型为探索肠道环境中局部 STEC-宿主相互作用和志贺毒素中毒的发病机制提供了一种新颖且有用的工具。
