二氧化硅增强小鼠对内毒素的敏感性。
Silica enhancement of murine endotoxin sensitivity.
作者信息
Vogel S N, English K E, O'Brien A D
出版信息
Infect Immun. 1982 Nov;38(2):681-5. doi: 10.1128/iai.38.2.681-685.1982.
Abstract
Silica has been used for many years as an agent which selectively alters macrophage functions and, as such, has been used to assess the role of macrophages in the immune response to a variety of microbial and chemically defined agents. Silica treatment of C3H/HeN mice 1 day before challenge with protein-free Escherichia coli endotoxin (lipopolysaccharide [LPS]) resulted in a marked increase in LPS sensitivity, as evidenced by accelerated signs of endotoxemia as well as a fourfold decrease in the LPS 50% lethal dose. The silica-mediated increase in responsiveness to LPS was associated with increased production of macrophage-derived soluble factors both in vivo (interferon) and in vitro (Interleukin 1; previously referred to as lymphocyte activating factor or LAF) upon endotoxin stimulation. These findings support the central role of the macrophage and its products in mediating endotoxic reactions.
摘要
多年来，二氧化硅一直被用作一种能选择性改变巨噬细胞功能的物质，因此，它被用于评估巨噬细胞在对多种微生物和化学物质的免疫反应中的作用。在用无蛋白大肠杆菌内毒素（脂多糖[LPS]）攻击前1天，对C3H/HeN小鼠进行二氧化硅处理，结果显示LPS敏感性显著增加，这表现为内毒素血症症状加速出现，以及LPS 50%致死剂量降低四倍。二氧化硅介导的对LPS反应性增加与内毒素刺激后体内（干扰素）和体外（白细胞介素1；以前称为淋巴细胞激活因子或LAF）巨噬细胞衍生的可溶性因子产生增加有关。这些发现支持了巨噬细胞及其产物在介导内毒素反应中的核心作用。
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