Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia.
Cancer Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria, Australia.
J Med Microbiol. 2020 Feb;69(2):290-297. doi: 10.1099/jmm.0.001163. Epub 2020 Jan 31.
is a recognised cause of foodborne intoxication and antibiotic-associated diarrhoea (AAD), which are both mediated by staphylococcal enterotoxins. However, unlike foodborne intoxication, AAD appears to require infection of the host. While intoxication is widely studied, little is known about pathogenesis in the context of gastrointestinal infection. To develop a mouse model of gastrointestinal infection. An established AAD mouse model was adapted for infection, and damage observed via histopathological analysis and immunostaining of intestinal tissues. Various strains colonised the mouse model, and analysis showed that although clinical signs of disease were not seen, infection induced damage in the small intestine, disrupting host structures essential for epithelial integrity. Studies using a staphylococcal enterotoxin B mutant showed that this toxin may contribute to damage during gastrointestinal infection. This work presents a new mouse model of gastrointestinal infection, while also providing insight into the pathogenesis of in the gut.
金黄色葡萄球菌是食源性中毒和抗生素相关性腹泻（AAD）的公认病因，这两者均由葡萄球菌肠毒素介导。然而，与食源性中毒不同的是，AAD 似乎需要宿主感染。虽然食源性中毒已广泛研究，但关于胃肠道感染中金黄色葡萄球菌的发病机制知之甚少。为了建立金黄色葡萄球菌胃肠道感染的小鼠模型，我们对现有的 AAD 小鼠模型进行了改造，通过对肠道组织进行组织病理学分析和免疫染色观察到损伤。各种菌株在小鼠模型中定植，分析表明，尽管未观察到疾病的临床症状，但金黄色葡萄球菌感染会导致小肠损伤，破坏宿主结构，对上皮完整性至关重要。使用金黄色葡萄球菌肠毒素 B 突变体的研究表明，这种毒素可能会导致胃肠道感染期间的损伤。这项工作提出了金黄色葡萄球菌胃肠道感染的新小鼠模型，同时也深入了解了金黄色葡萄球菌在肠道中的发病机制。
