半乳糖胺诱导的内毒素致敏中对脂多糖反应性巨噬细胞的需求。
Requirement for lipopolysaccharide-responsive macrophages in galactosamine-induced sensitization to endotoxin.
作者信息
Freudenberg M A, Keppler D, Galanos C
出版信息
Infect Immun. 1986 Mar;51(3):891-5. doi: 10.1128/iai.51.3.891-895.1986.
Abstract
Injection of D-galactosamine sensitizes mice many thousand-fold to the lethal action of endotoxin (lipopolysaccharide [LPS]). Comparable sensitization was practically absent in LPS-resistant C3H/HeJ mice, which after D-galactosamine treatment were about 500,000 times less sensitive to LPS lethality than histocompatible LPS-sensitive C3H/HeN mice. D-Galactosamine induces changes in the hepatocytes of treated animals, such as depletion of UTP and alterations in the pattern of UDP sugars. These early biochemical changes, which are necessary for development of sensitization, were similar in both mouse strains which we examined. High sensitivity to the lethal effects of LPS was achieved in C3H/HeJ mice after D-galactosamine treatment by transfer of C3H/HeN macrophages obtained in culture from bone marrow precursor cells.
摘要
注射D-半乳糖胺可使小鼠对内毒素（脂多糖[LPS]）的致死作用敏感数千倍。在LPS抗性C3H/HeJ小鼠中几乎不存在类似的致敏作用，D-半乳糖胺处理后，它们对LPS致死性的敏感性比组织相容性LPS敏感的C3H/HeN小鼠低约500,000倍。D-半乳糖胺可诱导经处理动物的肝细胞发生变化，如UTP耗竭和UDP糖模式改变。这些早期生化变化是致敏作用发展所必需的，在我们检测的两种小鼠品系中相似。通过转移从骨髓前体细胞培养获得的C3H/HeN巨噬细胞，D-半乳糖胺处理后的C3H/HeJ小鼠对LPS的致死作用产生了高敏感性。
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