Lipopolysaccharide and tumor necrosis factor-alpha synergy potentiate serum-dependent responses of rat macrophages

被引:3
作者
Fox, ES [1 ]
Wang, L [1 ]
Tracy, TF [1 ]
机构
[1] ST LOUIS UNIV,PEDIAT RES INST,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63110
来源
SHOCK | 1996年 / 5卷 / 06期
关键词
D O I
10.1097/00024382-199606000-00007
中图分类号
R4 [临床医学];
学科分类号
1002 [临床医学]; 100602 [中西医结合临床];
摘要
Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) are major mediators of sepsis and multiple organ failure. Serum-mediated macrophage activation requires lipopolysaccharide (LPS) and its serum binding protein, lipopolysaccharide binding protein as a ligand for the receptor CD14, This study was designed to determine whether cytokines participate in regulation of serum-mediated LPS activation. Rat macrophages were stimulated with LPS with and without TNF-alpha or IL-1 beta and activation was determined by detection of TNF-alpha by specific enzyme-linked immunosorbent assay or TNF-alpha mRNA by Northern blot analysis. The addition of TNF-alpha but not IL-1 beta, in the presence of serum, leads to potentiation of macrophage activation after LPS stimulation. This effect could be specifically inhibited by neutralization of LPS with polymyxin B or an antibody against TNF-alpha. This study shows that LPS and TNF-alpha synergize to potentiate serum-mediated macrophage activation, These results demonstrate another element of the control mechanism of cytokine secretion following macrophage activation in sepsis.
引用
收藏
页码:429 / 433
页数:5
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