在低剂量内毒素模型中实验性消除肿瘤坏死因子对生存率有不同影响。
Experimental elimination of tumor necrosis factor in low-dose endotoxin models has variable effects on survival.
作者信息
Franks A K, Kujawa K I, Yaffe L J
机构信息
Casualty Care Research Department, Naval Medical Research Institute, Bethesda, Maryland 20889-5055.
出版信息
Infect Immun. 1991 Aug;59(8):2609-14. doi: 10.1128/iai.59.8.2609-2614.1991.
Abstract
Tumor necrosis factor alpha (TNF) is thought to play a major role in the pathogenesis of septic shock. Anti-TNF antibody was preadministered in low-dose endotoxin lethality models in which BALB/c mice were challenged with small amounts of lipopolysaccharide following their sensitization with either carrageenan (CAR) or D-galactosamine (D-GalN). Although the antibody virtually eliminated circulating TNF in both the CAR and the D-GalN models, only the D-GalN model mice were afforded survival, adding to a growing body of evidence that substances other than TNF play a key role in endotoxin-induced lethality. Further examination of sera from these mice showed a much greater elevation of interleukin-6 levels in the CAR-sensitized group than in the D-GalN-sensitized group.
摘要
肿瘤坏死因子α（TNF）被认为在脓毒症休克的发病机制中起主要作用。在低剂量内毒素致死模型中预先给予抗TNF抗体，在该模型中，BALB/c小鼠在用角叉菜胶（CAR）或D-半乳糖胺（D-GalN）致敏后，再用少量脂多糖进行攻击。尽管该抗体在CAR和D-GalN模型中几乎消除了循环中的TNF，但只有D-GalN模型小鼠存活，这增加了越来越多的证据表明，除TNF外的其他物质在内毒素诱导的致死性中起关键作用。对这些小鼠血清的进一步检测显示，CAR致敏组的白细胞介素-6水平升高幅度比D-GalN致敏组大得多。
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本文引用的文献
1
THE INTERACTION BETWEEN CARRAGEENAN AND THE FIRST COMPONENT OF COMPLEMENT.
J Immunol. 1965 May;94:662-6.
2
Comparison of in vitro cell cytotoxic assays for tumor necrosis factor.
J Immunol Methods. 1984 Mar 30;68(1-2):167-75. doi: 10.1016/0022-1759(84)90147-9.
3
Carrageenan and delayed hypersensitivity. II. Activation of Hageman factor by carrageenan and its possible significance.
Proc Soc Exp Biol Med. 1969 Dec;132(3):1021-4. doi: 10.3181/00379727-132-34358.
4
Spectrum and possible mechanism of carrageenan cytotoxicity.
Am J Pathol. 1971 Aug;64(2):387-404.
5
The differential suppression of antigen, lymphokine and mitogen-induced delayed hypersensitivity-type skin reactions by carrageenan.
Int Arch Allergy Appl Immunol. 1973;44(3):409-21. doi: 10.1159/000230948.
6
An examination of the cytotoxic effects of silica on macrophages.
J Exp Med. 1966 Aug 1;124(2):141-54. doi: 10.1084/jem.124.2.141.
7
Requirement for lipopolysaccharide-responsive macrophages in galactosamine-induced sensitization to endotoxin.
Infect Immun. 1986 Mar;51(3):891-5. doi: 10.1128/iai.51.3.891-895.1986.
8
Passive immunization against cachectin/tumor necrosis factor protects mice from lethal effect of endotoxin.
Science. 1985 Aug 30;229(4716):869-71. doi: 10.1126/science.3895437.
9
Shock and tissue injury induced by recombinant human cachectin.
Science. 1986 Oct 24;234(4775):470-4. doi: 10.1126/science.3764421.
10
Inhibition of macrophage accessory cell function in casein-treated B6C3F1 mice.
J Immunol. 1987 Sep 15;139(6):1804-10.
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