肿瘤坏死因子α在小鼠对肺炎溶素缺陷型肺炎链球菌引起的菌血症的宿主反应中的作用。
Role of tumor necrosis factor alpha in the host response of mice to bacteremia caused by pneumolysin-deficient Streptococcus pneumoniae.
作者信息
Benton K A, VanCott J L, Briles D E
机构信息
Department of Microbiology, The University of Alabama at Birmingham, 35294, USA.
出版信息
Infect Immun. 1998 Feb;66(2):839-42. doi: 10.1128/IAI.66.2.839-842.1998.
Abstract
Pneumolysin-deficient mutant strains of Streptococcus pneumoniae are known to cause less-severe sepsis than wild-type pneumococcal strains that produce pneumolysin. This difference is associated with greater host resistance in mice infected with the pneumolysin-deficient strains. These studies show that the host resistance developed during the first 1 to 2 days after infection with a pneumolysin-deficient mutant strain is dependent on tumor necrosis factor alpha but is apparently independent of interleukin 1beta (IL-1beta) or IL-6. Survival beyond 5 days appeared to depend on the ability of the mice to produce IL-1beta.
摘要
已知肺炎链球菌的肺炎溶血素缺陷突变株引起的败血症比产生肺炎溶血素的野生型肺炎球菌菌株轻。这种差异与感染肺炎溶血素缺陷菌株的小鼠具有更强的宿主抵抗力有关。这些研究表明，感染肺炎溶血素缺陷突变株后1至2天内产生的宿主抵抗力依赖于肿瘤坏死因子α，但显然不依赖于白细胞介素1β（IL-1β）或IL-6。超过5天的存活似乎取决于小鼠产生IL-1β的能力。
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