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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Gamma Interferon Treatment of Patients with Chronic Granulomatous Disease Is Associated with Augmented Production of Nitric Oxide by Polymorphonuclear Neutrophils
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Gamma Interferon Treatment of Patients with Chronic Granulomatous Disease Is Associated with Augmented Production of Nitric Oxide by Polymorphonuclear Neutrophils

机译：γ干扰素治疗慢性肉芽肿病患者与多形核中性粒细胞增加一氧化氮的产生有关。

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Treatment with gamma-interferon (IFN-γ) is associated with reduced frequency and severity of infections in chronic granulomatous disease (CGD), but the mechanism is unknown. Since the inducible nitric oxide (NO) synthase can be amplified by IFN-γ in murine macrophages, for example, we hypothesized that IFN-γ might modulate NO release from polymorphonuclear neutrophils (PMNs) in patients with CGD. Eight patients with CGD and eight healthy controls were studied. Each patient was given either 50 or 100 μg of IFN-γ per m2 on two consecutive days. The production of NO fromN-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated PMNs was assessed as theN G-monomethyl-l-arginine-inhibitable oxidation of oxyhemoglobin to methemoglobin in the presence of catalase and superoxide dismutase. Prior to IFN-γ treatment, the PMNs from CGD patients produced 372 ± 27 (mean ± standard error of the mean) pmol of NO/106 PMNs at 45 min, while the control PMNs produced 343 ± 44 pmol. On day 1 after IFN-γ treatment, NO production increased to 132% ± 25% of that for controls, and on day 3 it reached 360% ± 37% (P < 0.001) of that for controls. On day 8, the values still remained higher, 280% ± 78% more than the control values. Likewise, the bactericidal capacity of PMNs increased on day 3. The present data show that IFN-γ treatment of CGD patients is associated with an increased production of NO from PMNs when activated by fMLP. Since these PMNs lack the capacity to produce superoxide anions, it is conceivable that this increase in NO release could be instrumental in augmenting host defense.
机译：γ-干扰素（IFN-γ）的治疗与慢性肉芽肿性疾病（CGD）的感染频率和严重程度降低有关，但机制尚不清楚。例如，由于IFN-γ可在鼠巨噬细胞中扩增可诱导型一氧化氮（NO）合酶，因此我们假设IFN-γ可能会调节CGD患者多形核中性粒细胞（PMN）的NO释放。研究了八名CGD患者和八名健康对照。每位患者连续两天每m 2 服用50或100μgIFN-γ。由 N -甲酰基-甲硫酰基-亮氨酰-苯丙氨酸（fMLP）刺激的PMN产生的NO评估为 N G -单甲基-在过氧化氢酶和超氧化物歧化酶的存在下，L-精氨酸可抑制氧合血红蛋白氧化为高铁血红蛋白。在进行IFN-γ治疗之前，CGD患者的PMN在45分钟时产生372±27（平均值±标准误差的平均值）pmol NO / 10 6 PMN，而对照PMN则产生343± 44 pmol。 IFN-γ处理后第1天，NO产量增加至对照的132％±25％，第3天达到对照的360％±37％（ P <0.001） 。在第8天，该值仍保持较高，比对照值高280％±78％。同样，PMNs的杀菌能力在第3天增加。目前的数据显示，当被fMLP激活时，对CGD患者进行IFN-γ治疗与PM​​N产生NO的增加有关。由于这些PMN缺乏产生超氧阴离子的能力，因此可以想象，NO释放的这种增加可能有助于增强宿主防御能力。

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