Role of tumor necrosis factor alpha in the host response of mice to bacteremia caused by pneumolysin-deficient Streptococcus pneumoniae

被引:29
作者
Benton, KA
VanCott, JL
Briles, DE
机构
[1] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA
[2] Univ Alabama, Dept Pediat, Birmingham, AL 35294 USA
[3] Univ Alabama, Dept Comparat Med, Birmingham, AL 35294 USA
关键词
D O I
10.1128/IAI.66.2.839-842.1998
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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,vith a pneumolysin deficient mutant strain is dependent on tumor necrosis factor alpha but is apparently independent of interleukin 1 beta (IL-1 beta) or IL-6. Survival beyond 5 days appeared to depend on the ability of the mice to produce IL-1 beta.
引用
收藏
页码:839 / 842
页数:4
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