白细胞介素1或肿瘤坏死因子可促进柯萨奇B3病毒诱导的抗性B10.A小鼠发生心肌炎。
Interleukin 1 or tumor necrosis factor can promote Coxsackie B3-induced myocarditis in resistant B10.A mice.
作者信息
Lane J R, Neumann D A, Lafond-Walker A, Herskowitz A, Rose N R
机构信息
Department of Immunology and Infectious Diseases, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205.
出版信息
J Exp Med. 1992 Apr 1;175(4):1123-9. doi: 10.1084/jem.175.4.1123.
Abstract
We have previously demonstrated that bacterial lipopolysaccharide (LPS) is capable of promoting Coxsackie B3 (CB3)-induced myocarditis in genetically resistant B10.A mice. Because LPS is known to increase production of various cytokines, we tested CB3-infected, LPS-treated mice for the presence of interleukin 1 (IL-1) and tumor necrosis factor (TNF). We found significantly increased amounts of both cytokines in the sera of CB3/LPS-treated mice compared with animals treated only with LPS. We also found immunohistochemical evidence for local production of these cytokines in the cardiac tissue of CB3/LPS-treated mice. Treatment with IL-1 or TNF alone promoted CB3-induced autoimmune myocarditis in resistant B10.A mice. Myocarditis was also observed when uninfected mice were immunized with syngeneic heart extract in the presence of IL-1 or TNF.
摘要
我们之前已经证明，细菌脂多糖（LPS）能够在基因抗性B10.A小鼠中促进柯萨奇B3（CB3）诱导的心肌炎。由于已知LPS会增加多种细胞因子的产生，我们检测了感染CB3且经LPS处理的小鼠体内白细胞介素1（IL-1）和肿瘤坏死因子（TNF）的存在情况。我们发现，与仅用LPS处理的动物相比，经CB3/LPS处理的小鼠血清中这两种细胞因子的含量显著增加。我们还发现了免疫组化证据，证明在经CB3/LPS处理的小鼠心脏组织中这些细胞因子是局部产生的。单独用IL-1或TNF处理可促进抗性B10.A小鼠发生CB3诱导的自身免疫性心肌炎。当未感染的小鼠在存在IL-1或TNF的情况下用同基因心脏提取物免疫时，也观察到了心肌炎。
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本文引用的文献
1
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Infect Immun. 1983 Sep;41(3):1157-65. doi: 10.1128/iai.41.3.1157-1165.1983.
2
Cardiac myosin induces myocarditis in genetically predisposed mice.心肌肌凝蛋白在具有遗传易感性的小鼠中诱发心肌炎。
J Immunol. 1987 Dec 1;139(11):3630-6.
3
Cachectin: more than a tumor necrosis factor.恶病质素：不仅仅是一种肿瘤坏死因子。
N Engl J Med. 1987 Feb 12;316(7):379-85. doi: 10.1056/NEJM198702123160705.
4
A short synthetic peptide fragment of human interleukin 1 with immunostimulatory but not inflammatory activity.一种具有免疫刺激活性但无炎症活性的人白细胞介素1的短合成肽片段。
J Immunol. 1986 Nov 15;137(10):3201-4.
5
In vivo administration with IL-1 accelerates the development of collagen-induced arthritis in mice.在小鼠体内给予白细胞介素-1可加速胶原诱导性关节炎的发展。
J Immunol. 1988 Aug 1;141(3):834-41.
6
Tumour necrosis factor as immunomodulator and mediator of monocyte cytotoxicity induced by itself, gamma-interferon and interleukin-1.肿瘤坏死因子作为免疫调节剂以及由其自身、γ-干扰素和白细胞介素-1诱导的单核细胞细胞毒性的介质。
Nature. 1986;323(6083):86-9. doi: 10.1038/323086a0.
7
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10
Cachectin and tumour necrosis factor as two sides of the same biological coin.恶病质素与肿瘤坏死因子是同一枚生物硬币的两面。
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