Regulation of tumour necrosis factor production by mouse peritoneal macrophages: the role of cellular cyclic AMP.
Regulation of tumour necrosis factor production by mouse peritoneal macrophages: the role of cellular cyclic AMP.
复制标题
小鼠腹腔巨噬细胞对肿瘤坏死因子产生的调节：细胞环磷酸腺苷的作用。
DOI：
10.1016/s0021-9258(18)71615-3
复制
发表时间：
1988
期刊：
影响因子：
6.4
通讯作者：
T. Fujita
中科院分区：
文献类型：
--
作者：
Y. Katakami;Y. Nakao;Tamio Koizumi;N. Katakami;R. Ogawa;T. Fujita
我们研究了环腺苷3′：5′单磷酸（cAMP）在调节脂多糖（LPS）诱导的小鼠腹腔巨噬细胞产生肿瘤坏死因子（TNF）中的作用。LPS不改变细胞内cAMP水平。然而，前列腺素E2 （PGE2）和霍乱毒素，这两者都是已知的增加细胞内cAMP水平，一直抑制lps诱导的TNF生成。cAMP类似物，二丁基cAMP （DbcAMP）和8-溴cAMP （8BrcAMP）也能抑制TNF的产生，而百日咳毒素灭活了抑制性鸟嘌呤核苷酸结合蛋白（Gi），却没有作用。这些观察结果表明，LPS本身并不改变巨噬细胞腺苷酸环化酶活性，而增加细胞内cAMP水平的药物能够抑制LPS诱导的巨噬细胞TNF的产生。
We have studied the role of cyclic adenosine 3':5' monophosphate (cAMP) in the regulation of lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF) production by mouse peritoneal macrophages. LPS did not alter the intracellular levels of cAMP. However, prostaglandin E2 (PGE2) and cholera toxin, both of which are known to increase intracellular levels of cAMP, consistently inhibited LPS-induced TNF production. The cAMP analogues, dibutyryl cAMP (DbcAMP) and 8-bromo cAMP (8BrcAMP), also inhibited TNF production, whereas pertussis toxin, which inactivates the inhibitory guanine nucleotide-binding protein (Gi), had no effect. These observations suggested that LPS did not itself modify macrophage adenylate cyclase activity, while agents that increased intracellular cAMP levels were able to inhibit LPS-induced macrophage TNF production.