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首页> 外文期刊>Journal of endotoxin research >D-galactosamine lethality model: scope and limitations.
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D-galactosamine lethality model: scope and limitations.

机译：D-半乳糖胺杀伤力模型：范围和局限性。

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D-Galactosamine (D-galN) is well established as sensitizing mice and other animals to the lethal effects of TNF, specifically, and by several orders of magnitude. Protection by anti-TNF neutralizing antibody is complete, as is (metabolically-based) protection by uridine. Sensitization occurs regardless of the origin of the released TNF, whether it is released from macrophages and/or T-cells. The same is true for the challenging agent which leads to the release of TNF, whether it is endotoxin, a superantigen, lipoprotein, bacterial DNA, or bacteria, either killed or proliferating. Most studies have utilized endotoxin as the challenging agent, and more than 70 agents have been reported to confer protection against LPS and/or TNF challenge in the model. The model has provided new insight regarding modes of protection, including from dexamethasone, which protects against challenge from LPS but not from challenge by TNF. The D-galN lethality model has also been used to test for synergistic behavior between different bacterial components, and to test for lethality when only small amounts of the challenging agent are available (lipid A chemistry).
机译：D-半乳糖胺（D-galN）已被广泛确立，可以使小鼠和其他动物对TNF的致死作用敏感，尤其是在几个数量级上。通过抗TNF中和抗体的保护已经完成，尿苷（基于代谢）的保护也是如此。不管释放的TNF的来源如何，是否从巨噬细胞和/或T细胞释放，都会发生致敏作用。对于导致TNF释放的挑战剂，无论是内毒素，超抗原，脂蛋白，细菌DNA还是被杀死或正在增殖的细菌，也是如此。大多数研究已将内毒素用作攻击剂，并且据报道，已有70多种药物在模型中提供了针对LPS和/或TNF攻击的保护作用。该模型提供了有关保护模式的新见解，包括地塞米松的保护模式，地塞米松可防止LPS攻击，但不能抵抗TNF攻击。 D-galN致死性模型也已用于测试不同细菌成分之间的协同行为，并在仅可使用少量挑战剂时测试致死性（脂质A化学）。

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