IL-6 functions as an exocrine hormone in inflammation. Hepatocytes undergoing acute phase responses require exogenous IL-6.
IL-6 functions as an exocrine hormone in inflammation. Hepatocytes undergoing acute phase responses require exogenous IL-6.
复制标题
IL-6 在炎症中充当外分泌激素。
DOI：
10.4049/jimmunol.144.10.3804
复制
发表时间：
1990
影响因子：
4.4
通讯作者：
Fey Gh
中科院分区：
文献类型：
--
作者：
J. Gauldie;W. Northemann;Fey Gh
我们以前已经表明，IL-6是主要的单核细胞和成纤维细胞衍生的急性时相蛋白基因的表达和肝细胞在炎症中的合成调节。最近，我们和其他人已经表明，大鼠和人类肝癌细胞表达IL-6 mRNA，并出现了问题，是否正常肝细胞表达IL-6，以及是否有任何这样的表达发生在正常的生理条件下，或在炎症中看到。Poly A+ mRNA从正常大鼠和从大鼠经历急性期反应的肝脏是不积极的，当探测与大鼠IL-6的cDNA的条件下，巨噬细胞的mRNA是强阳性。然后，我们比较了从正常大鼠新鲜分离的纯化肝细胞中的poly A+ mRNA--从正在经历急性炎症反应的大鼠和从在存在或不存在地塞米松（microM）的情况下培养24小时的新鲜分离的正常肝细胞中。只有在无糖皮质激素的情况下培养24 h的正常肝细胞的mRNA中IL-6明显阳性。γ-纤维蛋白原mRNA表达的增加表明存在炎症。这些结果证实了IL-6作为调节炎症中正常肝脏急性期蛋白合成的外源性激素的鉴定，并排除了在正常稳态下在肝脏中活跃的自分泌机制。
We have previously shown that IL-6 is the major monocyte- and fibroblast-derived regulator of acute phase protein gene expression and synthesis in hepatocytes in inflammation. Recently, we and others have shown that rat and human hepatoma cells express IL-6 mRNA, and the question arose as to whether normal hepatocytes express IL-6 and whether any such expression occurs under normal physiologic conditions or is seen in inflammation. Poly A+ mRNA of liver from normal rats and from rats undergoing an acute phase response was not positive when probed with cDNA for rat IL-6 under conditions in which macrophage mRNA was strongly positive. We then compared poly A+ mRNA from purified hepatocytes freshly isolated from normal rats--from rats that were undergoing an acute inflammatory response and from freshly isolated normal hepatocytes that had been cultured for 24 h in the presence or absence of dexamethasone (microM). Only the mRNA from normal hepatocytes cultured for 24 h in the absence of any glucocorticoid was obviously positive for IL-6. The increased expression of gamma-fibrinogen mRNA indicated the presence of inflammation. These results confirm the identification of IL-6 as an exogenous hormone for regulating normal hepatic acute phase protein synthesis in inflammation and rules out an autocrine mechanism being active in the liver in normal homeostasis.