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.
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。
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