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首页> 外文期刊>Infection and immunity >Necessity and sufficiency of beta interferon for nitric oxide production in mouse peritoneal macrophages.
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Necessity and sufficiency of beta interferon for nitric oxide production in mouse peritoneal macrophages.

机译：β干扰素在小鼠腹膜巨噬细胞中产生一氧化氮的必要性和充分性。

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Bacterial lipopolysaccharide and some cytokines can activate macrophages to secrete nitric oxide. Macrophage-derived nitric oxide is a key cytotoxic factor for microbicidal and tumoricidal processes. We report here that a monoclonal antibody specific for beta interferon inhibited lipopolysaccharide-induced nitric oxide production in thioglycolate-elicited C3HeB/FeJ peritoneal macrophages and macrophage-like cell line RAW 264.7. In addition, exogenous added beta interferon enabled lipopolysaccharide-hyporesponsive thioglycolate-elicited C3H/HeJ peritoneal macrophages to produce nitric oxide in response to lipopolysaccharide. These data support the concept that beta interferon provides an essential signal(s) for lipopolysaccharide-triggered nitric oxide production by mouse macrophages. Heat-killed Staphylococcus aureus, a gram-positive bacterium which was unable to initiate nitric oxide production in thioglycolate-elicited C3HeB/FeJ peritoneal macrophages in vitro, promoted nitric oxide formation in the presence of beta interferon, suggesting that beta interferon may be a general cofactor necessary for bacterium-derived stimulus-induced nitric oxide production in these macrophages. However, neither beta interferon nor tumor necrosis factor alpha, alone or in combination, triggered nitric oxide production in thioglycolate-elicited mouse peritoneal macrophages, demonstrating that these macrophage-derived cytokines, while necessary, were not sufficient by themselves for the induction of nitric oxide production in these cells. On the other hand, gamma interferon and tumor necrosis factor alpha acted together to induce nitric oxide production in vitro in the absence of lipopolysaccharide in thioglycolate-elicited mouse peritoneal macrophages, indicating that these two types of interferons provided different signals during the activation of these macrophages.
机译：细菌脂多糖和某些细胞因子可以激活巨噬细胞分泌一氧化氮。巨噬细胞来源的一氧化氮是杀微生物和杀肿瘤过程的关键细胞毒性因子。我们在这里报告，特异性针对β干扰素的单克隆抗体抑制硫代乙醇酸盐诱导的C3HeB / FeJ腹膜巨噬细胞和巨噬细胞样细胞系RAW 264.7中脂多糖诱导的一氧化氮的产生。另外，外源添加的β-干扰素能够使脂多糖低反应性巯基乙酸盐诱导的C3H / HeJ腹膜巨噬细胞产生一氧化氮，以响应脂多糖。这些数据支持以下概念：β干扰素为小鼠巨噬细胞产生脂多糖触发的一氧化氮产生提供了必要的信号。热灭活的金黄色葡萄球菌是一种革兰氏阳性细菌，无法在硫代乙醇酸盐诱导的C3HeB / FeJ腹膜巨噬细胞中引发一氧化氮的产生，在存在β干扰素的情况下促进了一氧化氮的形成，这表明β干扰素可能是一种普遍现象这些巨噬细胞中细菌衍生的刺激诱导的一氧化氮产生所必需的辅因子。但是，无论是β干扰素还是肿瘤坏死因子α单独或联合使用都不会在硫代乙醇酸酯诱导的小鼠腹膜巨噬细胞中触发一氧化氮的产生，表明这些巨噬细胞衍生的细胞因子虽然必要，但不足以诱导一氧化氮的产生。这些细胞中的生产。另一方面，在巯基乙酸盐诱导的小鼠腹膜巨噬细胞中不存在脂多糖的情况下，γ干扰素和肿瘤坏死因子α共同在体外诱导一氧化氮的产生，表明这两种干扰素在这些巨噬细胞激活期间提供了不同的信号。 。

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