Effect of recombinant interleukin-1beta on murine CD14 gene expression in vivo.
Effect of recombinant interleukin-1beta on murine CD14 gene expression in vivo.
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重组白细胞介素1β对体内小鼠CD14基因表达的影响。
DOI：
10.1097/00024382-199803000-00001
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Ulevitch,RJ
中科院分区：
文献类型：
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作者：
Fearns,C;Ulevitch,RJ
重组鼠白细胞介素-1β(IL-1β)诱导血浆CD14水平短暂增加，并在8小时达到峰值，并且血浆CD14抗原的增加伴随着所有检查器官中CD14信使核糖核酸(mRNA)水平的增加。在大多数器官中，在施用125ng IL-1β后获得最大水平的诱导。此外，原位杂交研究表明，CD14 mRNA 在骨髓细胞和上皮细胞中均被诱导。用抗IL-1β抗体预处理小鼠降低了脂多糖(LPS)随后诱导的CD14血浆水平，并显着降低了肾脏和肝脏中CD14 mRNA的诱导水平。抗体不会阻断 LPS 介导的肺诱导作用。用抗IL-1β和抗肿瘤坏死因子(TNF)抗体的组合进行预处理比单独用任一抗体进行预处理在减少LPS介导的血浆CD14和肝脏中CD14 mRNA的诱导方面更有效。抗IL-1β和抗TNF抗体的组合在肾和肺中没有比单独使用抗TNF观察到的额外效果。这些研究表明体内LPS对CD14基因表达的调节涉及多种信号，但部分是由细胞因子IL-1β和TNF-α介导的。
Recombinant murine interleukin-1 [beta](IL-1 [beta]) induced a transient increase in plasma levels of CD14 with a peak at 8 h, and this increase in plasma CD14 antigen was accompanied by increased levels of CD14 messenger ribonucleic acid (mRNA) in all organs examined. In most organs, maximal levels of induction were obtained after administration of 125 ng of IL-1 [beta]. Moreover, in situ hybridization studies revealed that CD14 mRNA was induced in both myeloid cells and epithelial cells. Pretreatment of mice with anti-IL-1 [beta] antibodies reduced the subsequent induction of plasma levels of CD14 by lipopolysaccharide (LPS) and significantly reduced the level of induction of CD14 mRNA in kidney and liver. The antibodies did not block LPS mediated induction in lung. Pretreatment with a combination of anti-IL-1 [beta] and anti-tumor necrosis factor (TNF) antibodies was more effective in reducing LPS mediated induction of plasma CD14 and CD14 mRNA in liver than pretreatment with either antibody alone. The combination of anti-IL-1 [beta] and anti-TNF antibodies had no additional effect in kidney and lung over that observed with anti-TNF alone. These studies demonstrate that regulation of CD14 gene expression by LPS in vivo involves multiple signals but is mediated, in part, by the cytokines IL-1 [beta] and TNF-[alpha].