Alveolar macrophages autoregulate IL-1 and IL-6 production by endogenous nitric oxide
Alveolar macrophages autoregulate IL-1 and IL-6 production by endogenous nitric oxide
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DOI：
10.1165/ajrcmb.14.3.8845178
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发表时间：
1996-03-01
影响因子：
6.4
通讯作者：
Kraal, G
中科院分区：
文献类型：
--
作者：
Persoons, JHA;Schornagel, K;Kraal, G
研究了一氧化氮对脂多糖（LPS）诱导的肺泡巨噬细胞产生细胞因子的影响。当培养肺泡巨噬细胞时，在用LPS刺激时产生大量的白细胞介素-1（IL-1）、白细胞介素-6（IL-6）、肿瘤坏死因子α（TNF-α）和一氧化氮。通过L-精氨酸类似物N-G-单甲基-L-精氨酸（NMMA）抑制一氧化氮产生，导致IL-1 β和IL-6增加，而TNF-α浓度保持不变，表明一氧化氮对肺泡巨噬细胞LPS刺激的细胞因子产生的特异性抑制作用。所观察到的精氨酸调节特性的一氧化氮没有导致细胞毒性作用的L-精氨酸对巨噬细胞的氧化，因为一氧化氮的合成不影响肺泡巨噬细胞的活力。相反，一氧化氮供体S-亚硝基-N-乙酰基-D，L-青霉胺（SNAP）诱导LPS刺激的肺泡巨噬细胞中IL-1产生的剂量依赖性抑制，其中内源性一氧化氮产生被阻断。结果表明，一氧化氮可以影响LPS诱导的IL-1 β和IL-6分泌的肺泡巨噬细胞在自动调节的方式和讨论的重要生理后果，这种自动调节一氧化氮可能有。
The effect of nitric oxide on the lipopolysaccharide (LPS)-induced cytokine production by alveolar macrophages was studied. When alveolar macrophages were cultured, substantial amounts of interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and nitric oxide are produced upon stimulation with LPS. Inhibition of the nitric oxide production by the L-arginine analogue N-G-monomethyl-L-arginine (NMMA), resulted in an increase of IL-1 beta and IL-6, whereas the TNF-alpha concentrations remained unchanged, suggesting specific inhibitory effects of nitric oxide on the LPS-stimulated cytokine production by alveolar macrophages. The observed cytokine-modulating properties of nitric oxide did not result from cytotoxic actions of the oxidation of L-arginine on macrophages, since nitric oxide synthesis did not affect the viability of the alveolar macrophages. Conversely the nitric oxide donor S-nitroso-N-acetyl-D, L-penicillamine (SNAP) induced dose-dependent inhibition of IL-1 production in LPS-stimulated alveolar macrophages in which endogenous nitric oxide production was blocked. The results indicate that nitric oxide can affect the LPS-induced IL-1 beta and IL-6 secretion by alveolar macrophages in an autoregulatory way and are discussed in view of the important physiologic consequences this autoregulation by nitric oxide may have.