Inhaled corticosteroids increase interleukin-10 but reduce macrophage inflammatory protein-1α, granulocyte-macrophage colony-stimulating factor, and interferon-γ release from alveolar macrophages in asthma
Inhaled corticosteroids increase interleukin-10 but reduce macrophage inflammatory protein-1α, granulocyte-macrophage colony-stimulating factor, and interferon-γ release from alveolar macrophages in asthma
复制标题
DOI：
10.1164/ajrccm.157.1.9703079
复制
发表时间：
1998-01-01
影响因子：
24.7
通讯作者：
Chung, KF
中科院分区：
文献类型：
--
作者：
John, M;Lim, S;Chung, KF
在一项双盲交叉安慰剂对照研究中，我们测定了吸入皮质类固醇布地奈德对轻度哮喘患者单核细胞和肺泡巨噬细胞释放抗炎细胞因子白介素10(IL-10)和促炎细胞因子巨噬细胞炎性蛋白-1α(MIP-1α)、干扰素-γ(干扰素-γ)和粒细胞-巨噬细胞集落刺激因子(GM-CSF)的影响。布地奈德降低了支气管高反应性，改善了基线FEV1。在每个治疗阶段结束时，通过支气管肺泡灌洗获得肺泡巨噬细胞。经糖皮质激素治疗后，单核细胞IL-10的表达无明显变化，但内毒素和IL-1β刺激的肺泡巨噬细胞IL-10mRNA和蛋白表达均增加。相比之下，经类固醇治疗后，肺泡巨噬细胞释放的MIP-1α、干扰素-γ和GM-CSF显著减少。与正常非哮喘志愿者的肺泡巨噬细胞相比，哮喘患者的肺泡巨噬细胞释放更多的MIP-1α、干扰素-γ和GM-CSF，而释放更少的IL-10，尤其是在基线和IL-1β刺激后。类固醇抑制促炎细胞因子的能力，但增强抗炎细胞因子，如IL-10的能力可能有助于它们在哮喘中的有益作用。哮喘的特征是肺泡巨噬细胞释放促炎细胞因子的能力增强，而产生IL-10的能力降低。
We determined the effect of inhaled corticosteroid, budesonide, on the release of the anti-inflammatory cytokine, interleukin-10 (IL-10), and of pro-inflammatory cytokines, macrophage inflammatory protein-1 alpha (MIP-1 alpha), interferon-gamma (IFN-gamma), and granulocyte-macrophage colony-stimulating factor (GM-CSF), from blood monocytes and alveolar macrophages of mild asthmatic subjects in a double-blind, cross-over, placebo-controlled study. Budesonide reduced bronchial hyperresponsiveness and improved baseline FEV1. Alveolar macrophages were obtained by bronchoalveolar lavage performed at the end of each treatment phase. IL-10 from blood monocytes was not altered, but both IL-10 mRNA and protein expression from alveolar macrophages stimulated by lipopolysaccharide and IL-1 beta were increased after corticosteroid therapy. By contrast, alveolar macrophages released significantly less MIP-1 alpha, IFN-gamma, and GM-CSF after steroid treatment. In comparison to alveolar macrophages from normal nonasthmatic volunteers, those from asthmatic patients released more MIP-1 alpha, IFN-gamma, and GM-CSF but lower amounts of IL-10 particularly at baseline and after IL-1 beta stimulation. The ability of steroids to inhibit pro-inflammatory cytokines but to enhance the anti-inflammatory cytokine such as IL-10 may contribute to their beneficial actions in asthma. Asthma is characterized by alveolar macrophages exhibiting both an enhanced capacity to release pro-inflammatory cytokines and a reduced capacity to produce IL-10.