肿瘤坏死因子α在小鼠肺炎球菌肺炎发病机制中的作用。
Role of tumor necrosis factor alpha in pathogenesis of pneumococcal pneumonia in mice.
作者信息
Takashima K, Tateda K, Matsumoto T, Iizawa Y, Nakao M, Yamaguchi K
机构信息
Department of Microbiology, Toho University School of Medicine, Tokyo, Japan.
出版信息
Infect Immun. 1997 Jan;65(1):257-60. doi: 10.1128/iai.65.1.257-260.1997.
Abstract
The production and role of tumor necrosis factor alpha (TNF-alpha) in pneumococcal pneumonia were investigated in a mouse pneumonia model. When approximately 10(6) CFU of Streptococcus pneumoniae TUM19 were used to inoculate CBA/J mice intranasally, TNF-alpha levels in the lungs and serum began to increase from 1 and 3 days after infection, respectively, concomitantly with the increase in bacterial counts in the lungs. Anti-TNF-alpha antibody accelerated bacterial proliferation in the blood and the death of the mice. Although serum levels of immunoglobulin G antibody against the infecting bacteria were not affected by the anti-TNF-alpha antibody treatment, neutrophil counts in the blood were decreased by the treatment. These results suggest that TNF-alpha produced in the course of pneumococcal pneumonia prevents bacteremia by increasing the number of neutrophils in the blood.
摘要
在小鼠肺炎模型中研究了肿瘤坏死因子α（TNF-α）在肺炎球菌肺炎中的产生及作用。当使用约10⁶CFU的肺炎链球菌TUM19经鼻接种CBA/J小鼠时，肺和血清中的TNF-α水平分别在感染后1天和3天开始升高，同时肺内细菌数量增加。抗TNF-α抗体加速了血液中细菌的增殖和小鼠的死亡。尽管抗TNF-α抗体治疗对感染细菌的免疫球蛋白G抗体血清水平没有影响，但该治疗使血液中的中性粒细胞计数减少。这些结果表明，肺炎球菌肺炎过程中产生的TNF-α通过增加血液中的中性粒细胞数量来预防菌血症。
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