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1
Streptococcus mitis cell walls and lipopolysaccharide induce lethality in D-galactosamine-sensitized mice by a tumor necrosis factor-dependent pathway.缓症链球菌细胞壁和脂多糖通过肿瘤坏死因子依赖性途径在D-半乳糖胺致敏小鼠中诱导致死性。
Infect Immun. 1996 May;64(5):1846-9. doi: 10.1128/iai.64.5.1846-1849.1996.
2
Tumor necrosis factor alpha mediates lethal activity of killed gram-negative and gram-positive bacteria in D-galactosamine-treated mice.肿瘤坏死因子α介导经D-半乳糖胺处理的小鼠中杀死的革兰氏阴性菌和革兰氏阳性菌的致死活性。
Infect Immun. 1991 Jun;59(6):2110-5. doi: 10.1128/iai.59.6.2110-2115.1991.
3
Induction of lethal shock and tolerance by Porphyromonas gingivalis lipopolysaccharide in D-galactosamine-sensitized C3H/HeJ mice.牙龈卟啉单胞菌脂多糖在D-半乳糖胺致敏的C3H/HeJ小鼠中诱导致死性休克和耐受性
Infect Immun. 1999 Jul;67(7):3399-402. doi: 10.1128/IAI.67.7.3399-3402.1999.
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Bacterial lipoprotein and lipopolysaccharide act synergistically to induce lethal shock and proinflammatory cytokine production.细菌脂蛋白和脂多糖协同作用，诱导致死性休克和促炎细胞因子产生。
J Immunol. 1997 Nov 15;159(10):4868-78.
5
LPS challenge in D-galactosamine-sensitized mice accounts for caspase-dependent fulminant hepatitis, not for septic shock.在D-半乳糖胺致敏小鼠中，脂多糖激发导致的是依赖半胱天冬酶的暴发性肝炎，而非败血性休克。
Am J Respir Crit Care Med. 1999 Apr;159(4 Pt 1):1308-15. doi: 10.1164/ajrccm.159.4.9712012.
6
Interleukin 10 reduces lethality and hepatic injury induced by lipopolysaccharide in galactosamine-sensitized mice.白细胞介素10可降低半乳糖胺致敏小鼠中脂多糖诱导的致死率和肝损伤。
Gastroenterology. 1996 Sep;111(3):736-44. doi: 10.1053/gast.1996.v111.pm8780580.
7
Apoptotic cell death in the response of D-galactosamine-sensitized mice to lipopolysaccharide as an experimental endotoxic shock model.以D-半乳糖胺致敏小鼠对脂多糖的反应作为实验性内毒素休克模型时的凋亡性细胞死亡
Infect Immun. 1996 Mar;64(3):734-8. doi: 10.1128/iai.64.3.734-738.1996.
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Porphyromonas gingivalis virulence in mice: induction of immunity to bacterial components.牙龈卟啉单胞菌在小鼠中的毒力：对细菌成分免疫的诱导
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Role of nitric oxide in lipopolysaccharide-induced hepatic injury in D-galactosamine-sensitized mice as an experimental endotoxic shock model.一氧化氮在D-半乳糖胺致敏小鼠脂多糖诱导的肝损伤中的作用：实验性内毒素休克模型
Infect Immun. 1999 Mar;67(3):1018-24. doi: 10.1128/IAI.67.3.1018-1024.1999.
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Involvement of tumor necrosis factor-alpha in development of hepatic injury in galactosamine-sensitized mice.肿瘤坏死因子-α在半乳糖胺致敏小鼠肝损伤发展中的作用。
Hepatology. 1990 Nov;12(5):1187-91. doi: 10.1002/hep.1840120518.

引用本文的文献

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Anomalous role of tumor necrosis factor alpha in experimental enterococcal infection.肿瘤坏死因子α在实验性肠球菌感染中的异常作用。
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Interaction of cationic peptides with lipoteichoic acid and gram-positive bacteria.阳离子肽与脂磷壁酸及革兰氏阳性菌的相互作用。
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本文引用的文献

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Endotoxic properties associated with cell walls of group A streptococci.与A组链球菌细胞壁相关的内毒素特性。
J Infect Dis. 1961 Jan-Feb;108:25-34. doi: 10.1093/infdis/108.1.25.
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Toxicity of recombinant toxic shock syndrome toxin 1 and mutant toxins produced by Staphylococcus aureus in a rabbit infection model of toxic shock syndrome.重组中毒性休克综合征毒素1及金黄色葡萄球菌产生的突变毒素在中毒性休克综合征兔感染模型中的毒性
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Gram-positive organisms and sepsis.革兰氏阳性菌与败血症
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Cytokine induction by extracellular products of oral viridans group streptococci.口腔草绿色链球菌细胞外产物诱导细胞因子产生
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Serum-induced potentiation of tumor necrosis factor alpha production by human monocytes in response to staphylococcal peptidoglycan: involvement of different serum factors.血清诱导人单核细胞对葡萄球菌肽聚糖产生肿瘤坏死因子α的增强作用：不同血清因子的参与
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Bacteremia due to viridans streptococcus in neutropenic patients with cancer: clinical spectrum and risk factors.癌症中性粒细胞减少患者的草绿色链球菌菌血症：临床谱及危险因素
Clin Infect Dis. 1994 Jan;18(1):25-31. doi: 10.1093/clinids/18.1.25.
7
Immunopathological activities of extracellular products of Streptococcus mitis, particularly a superantigenic fraction.缓症链球菌细胞外产物的免疫病理活性，特别是超抗原组分的免疫病理活性。
Infect Immun. 1995 Mar;63(3):785-93. doi: 10.1128/iai.63.3.785-793.1995.
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CD14 is a pattern recognition receptor.CD14是一种模式识别受体。
Immunity. 1994 Sep;1(6):509-16. doi: 10.1016/1074-7613(94)90093-0.
9
Soluble peptidoglycan-induced monokine production can be blocked by anti-CD14 monoclonal antibodies and by lipid A partial structures.可溶性肽聚糖诱导的单核因子产生可被抗CD14单克隆抗体和脂多糖A部分结构所阻断。
Infect Immun. 1994 Nov;62(11):4709-15. doi: 10.1128/iai.62.11.4709-4715.1994.
10
Gram-positive cell walls stimulate synthesis of tumor necrosis factor alpha and interleukin-6 by human monocytes.革兰氏阳性菌细胞壁可刺激人类单核细胞合成肿瘤坏死因子α和白细胞介素-6。
Infect Immun. 1994 Jul;62(7):2715-21. doi: 10.1128/iai.62.7.2715-2721.1994.

缓症链球菌细胞壁和脂多糖通过肿瘤坏死因子依赖性途径在D-半乳糖胺致敏小鼠中诱导致死性。

Streptococcus mitis cell walls and lipopolysaccharide induce lethality in D-galactosamine-sensitized mice by a tumor necrosis factor-dependent pathway.

作者信息

Le Roy D, Morand P, Lengacher S, Celio M, Grau G E, Glauser M P, Heumann D

机构信息

Department of Medicine, CHUV-Lausanne, Switzerland.

出版信息

Infect Immun. 1996 May;64(5):1846-9. doi: 10.1128/iai.64.5.1846-1849.1996.

DOI:10.1128/iai.64.5.1846-1849.1996
PMID:8613401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC174002/
Abstract

Purified cells walls of Streptococcus mitis induced tumor necrosis factor in vitro in whole blood of both lipopolysaccharide (LPS)-sensitive OF1 and LPS-resistant C3H/HeJ mice. They were as effective as heat-killed bacteria in inducing death in both strains of mice sensitized with D-galactosamine. Lethality was suppressed by anti-tumor necrosis factor antibodies. The histopathophysiological findings in mice after challenge with LPS or gram-positive cell walls were indistinguishable.

摘要

缓症链球菌的纯化细胞壁可在体外诱导脂多糖（LPS）敏感的OF1小鼠和LPS耐受的C3H/HeJ小鼠全血中的肿瘤坏死因子产生。在D-半乳糖胺致敏的两种小鼠品系中，它们诱导死亡的效果与热灭活细菌相同。抗肿瘤坏死因子抗体可抑制致死性。用LPS或革兰氏阳性细胞壁攻击后小鼠的组织病理生理学结果无明显差异。