Corraliza I M, Soler G, Eichmann K, Modolell M
Depto. de Bioquímica y Biología Molecular, Facultad de Veterinaria, Universidad de Extremadura, Cáceres, Spain.
Biochem Biophys Res Commun. 1995 Jan 17;206(2):667-73. doi: 10.1006/bbrc.1995.1094.
The present study addresses the regulatory mechanisms involved in the arginine metabolism of macrophages by arginase and nitric oxide synthase. Induction of both enzymes with LPS or by mixed lymphocyte reaction has been reported. Here, we demonstrate that these enzymes can be independently induced in murine bone-marrow-derived macrophages with the appropriate agonists. Arginase expression is specifically triggered by IL-4, IL-10, PGE2 as well as non-toxic or detoxified LPS. Conversely, IFN gamma induces only NO synthesis in these cells. The results demonstrate that the metabolism of arginine in macrophages is controlled by TH1/TH2-dependent cytokines and suggest a regulatory role of arginase on the NO synthesis by intracellular substrate depletion.
本研究探讨了精氨酸酶和一氧化氮合酶参与巨噬细胞精氨酸代谢的调控机制。已有报道称脂多糖（LPS）或混合淋巴细胞反应可诱导这两种酶的产生。在此，我们证明，使用适当的激动剂可在小鼠骨髓来源的巨噬细胞中独立诱导这些酶。精氨酸酶的表达由白细胞介素-4（IL-4）、白细胞介素-10（IL-10）、前列腺素E2（PGE2）以及无毒或解毒的LPS特异性触发。相反，γ干扰素（IFNγ）仅在这些细胞中诱导一氧化氮（NO）的合成。结果表明，巨噬细胞中精氨酸的代谢受TH1/TH2依赖性细胞因子的控制，并提示精氨酸酶通过细胞内底物耗竭对NO合成具有调节作用。
