Division of Toxicology, Office of Applied Research and Safety Assessment, Center for Food Safety and Applied Nutrition, US Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708, USA.
Commissioner's Fellowship Program, Division of Toxicology, Office of Applied Research and Safety Assessment, Center for Food Safety and Applied Nutrition, US Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708, USA.
Toxins (Basel). 2014 Apr 25;6(5):1471-89. doi: 10.3390/toxins6051471.
The staphylococcal enterotoxins (SEs) are the products of Staphylococcus aureus and are recognized as the causative agents of classical food poisoning in humans following the consumption of contaminated food. While illness evoked by ingestion of the SE or its producer organism in tainted food are often self-limited, our current understanding regarding the evolution of S. aureus provokes the utmost concern. The organism and its associated toxins, has been implicated in a wide variety of disease states including infections of the skin, heart, sinuses, inflammatory gastrointestinal disease, toxic shock, and Sudden Infant Death Syndrome. The intricate relationship between the various subsets of immunocompetent T cells and accessory cells and the ingested material found within the gastrointestinal tract present daunting challenges to the maintenance of immunologic homeostasis. Dysregulation of the intricate balances within this environment has the potential for extreme consequences within the host, some of which are long-lived. The focus of this review is to evaluate the relevance of staphylococcal enterotoxin in the context of mucosal immunity, and the underlying mechanisms that contribute to the pathogenesis of gastrointestinal autoimmune disease.
葡萄球菌肠毒素（SEs）是金黄色葡萄球菌的产物，被认为是人类食用污染食物后引发经典食物中毒的病原体。虽然摄入 SE 或其产生菌污染的食物引起的疾病通常是自限性的，但我们目前对金黄色葡萄球菌进化的认识引起了极大的关注。该生物体及其相关毒素已被牵连到多种疾病状态，包括皮肤、心脏、鼻窦、炎症性胃肠道疾病、中毒性休克和婴儿猝死综合征。各种免疫功能正常的 T 细胞亚群和辅助细胞与胃肠道内摄入的物质之间的复杂关系，给维持免疫稳态带来了巨大的挑战。这种环境中错综复杂的平衡失调，有可能对宿主造成极端后果，其中一些后果是长期存在的。本综述的重点是评估肠毒素在黏膜免疫中的相关性，以及导致胃肠道自身免疫性疾病发病机制的潜在机制。
