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。
Regulation of tumour necrosis factor production by mouse peritoneal macrophages: the role of cellular cyclic AMP.
作者信息
Katakami Y, Nakao Y, Koizumi T, Katakami N, Ogawa R, Fujita T
机构信息
Department of Medicine, Kobe University School of Medicine, Japan.
出版信息
Immunology. 1988 Aug;64(4):719-24.
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.
我们研究了环磷腺苷（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并未改变细胞内cAMP的水平。然而，已知均可增加细胞内cAMP水平的前列腺素E2（PGE2）和霍乱毒素，始终抑制LPS诱导的TNF产生。cAMP类似物，二丁酰cAMP（DbcAMP）和8-溴cAMP（8BrcAMP）也抑制TNF产生，而使抑制性鸟嘌呤核苷酸结合蛋白（Gi）失活的百日咳毒素则无作用。这些观察结果表明，LPS本身并未改变巨噬细胞腺苷酸环化酶活性，而增加细胞内cAMP水平的试剂能够抑制LPS诱导的巨噬细胞TNF产生。
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