Lipopolysaccharide and tumor necrosis factor-alpha synergy potentiate serum-dependent responses of rat macrophages.
Lipopolysaccharide and tumor necrosis factor-alpha synergy potentiate serum-dependent responses of rat macrophages.
复制标题
脂多糖和肿瘤坏死因子-α 协同作用增强大鼠巨噬细胞的血清依赖性反应。
DOI：
10.1097/00024382-199606000-00007
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
TracyJr,TF
中科院分区：
文献类型：
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作者：
Fox,ES;Wang,L;TracyJr,TF
肿瘤坏死因子-+/-（TNF-+/-）和白细胞介素-1 +/-（IL-1+/-）是脓毒症和多器官衰竭的主要介质。血清介导的巨噬细胞活化需要脂多糖（LPS）及其血清结合蛋白，脂多糖结合蛋白作为受体CD 14的配体。本研究旨在确定细胞因子是否参与调节血清介导的LPS活化。用含和不含TNF-+/-或IL-1+/-的LPS刺激大鼠巨噬细胞，并通过特异性酶联免疫吸附试验检测TNF-+/-或通过北方印迹分析检测TNF-+/-mRNA来确定活化。在血清存在下，加入TNF-+/-而不是IL-1+/-导致LPS刺激后巨噬细胞活化增强。这种作用可以通过用多粘菌素B或抗TNF-+/-的抗体中和LPS来特异性抑制。该研究表明，LPS和TNF-+/-协同增强血清介导的巨噬细胞活化。这些结果证明了脓毒症中巨噬细胞活化后细胞因子分泌控制机制的另一个要素。
Tumor necrosis factor-+/-(TNF-+/-) and interleukin-1+/-(IL-1+/-) 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-+/-or IL-1+/-and activation was determined by detection of TNF-+/-by specific enzyme-linked immunosorbent assay or TNF-+/-mRNA by Northern blot analysis. The addition of TNF-+/-but not IL-1+/-, 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-+/-. This study shows that LPS and TNF-+/-synergize to potentiate serum-mediated macrophage activation. These results demonstrate another element of the control mechanism of cytokine secretion following macrophage activation in sepsis.