内源性白细胞介素-6通过抑制肿瘤坏死因子α的产生，在链球菌中毒性休克综合征中发挥关键的保护作用。
Endogenous interleukin-6 plays a crucial protective role in streptococcal toxic shock syndrome via suppression of tumor necrosis factor alpha production.
作者信息
Diao Hongyan, Kohanawa Masashi
机构信息
Division of Molecular Immunology, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 0600815, Japan.
出版信息
Infect Immun. 2005 Jun;73(6):3745-8. doi: 10.1128/IAI.73.6.3745-3748.2005.
Abstract
During a Streptococcus pyogenes infection in interleukin-6 (IL-6)-deficient mice, there is elevation of serum tumor necrosis factor alpha (TNF-alpha) levels, muscular necrosis, and death compared with infection of C57BL/6 mice. Anti-TNF-alpha monoclonal antibody treatment decreased mortality and muscular necrosis in the infected IL-6-deficient mice. These results suggest that IL-6 plays a crucial protective role via suppression of TNF-alpha production in S. pyogenes infection.
摘要
在白细胞介素-6（IL-6）缺陷小鼠感染化脓性链球菌期间，与C57BL/6小鼠感染相比，血清肿瘤坏死因子α（TNF-α）水平升高、出现肌肉坏死并导致死亡。抗TNF-α单克隆抗体治疗降低了感染的IL-6缺陷小鼠的死亡率和肌肉坏死。这些结果表明，在化脓性链球菌感染中，IL-6通过抑制TNF-α的产生发挥关键的保护作用。
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