Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma.
Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma.
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卵白蛋白诱导的哮喘小鼠模型中肺间质巨噬细胞极化的表型转变
DOI：
10.3892/etm.2017.4699
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发表时间：
2017-08
影响因子：
2.7
通讯作者：
Hu S
中科院分区：
文献类型：
--
作者：
Nie H;Wang A;He Q;Yang Q;Liu L;Zhang G;Huang Y;Ding X;Yu H;Hu S
巨噬细胞的表型和功能根据其极化状态而变化，这反过来又取决于微环境刺激。在正常生理条件下，表达白细胞介素（IL）-10的肺间质巨噬细胞被认为在预防气道过敏反应中起调节作用。然而，在哮喘的病理生理过程中，肺间质巨噬细胞的表型特征仍然未知。在本研究中，肺间质巨噬细胞的表型特征进行了研究，在卵清蛋白（OVA）诱导的哮喘小鼠模型。采用流式细胞术、逆转录-定量聚合酶链反应、免疫印迹分析和ELISA检测肺间质巨噬细胞表面标志物趋化因子配体和白细胞介素的模式以及代谢酶活性。结果表明，哮喘小鼠肺间质巨噬细胞表达与交替活化巨噬细胞（M2）相关的表型标志物，包括分化簇-206、转氨酶2、精氨酸酶（Arg）1和趋化因子配体（CCL）17/CCL 22/CCL 24分泌。M2巨噬细胞还表现出Arg 1活性水平增加和IL-10表达水平降低，相对于来自对照小鼠的巨噬细胞。然而，当评价与经典活化（M1）巨噬细胞相关的标志物（即诱导型一氧化氮合酶和IL-12）的表达时，观察到哮喘小鼠间质巨噬细胞中M1标志物的水平与对照组无显著差异。总的来说，这些数据表明，肺间质巨噬细胞经历了一个表型转换，从正常条件下的调节巨噬细胞表型到OVA诱导的哮喘小鼠的另一种活化状态。
Macrophage phenotype and function varies according to their polarized state, which in turn is dependent on microenvironmental stimuli. Under normal physiological conditions, lung interstitial macrophages that express interleukin (IL)-10 are considered to serve regulatory roles in the prevention of allergic reactions in the airways. However, the phenotypic profile of lung interstitial macrophages during the pathophysiology of asthma remains unknown. In the current study, the phenotypic characteristics of lung interstitial macrophages were investigated in an ovalbumin (OVA)-induced mouse model of asthma. The patterns of surface markers chemokine ligand and interleukin, and the metabolic enzyme activity of lung interstitial macrophages were investigated using flow cytometry analysis, reverse transcription-quantitative polymerase chain reaction, western blot analysis, and ELISA. It was observed that lung interstitial macrophages derived from OVA-induced asthmatic mice expressed phenotypic markers associated with alternatively activated macrophages (M2), including cluster of differentiation-206, transglutaminase 2, arginase (Arg) 1 and chemokine ligand (CCL)17/CCL22/CCL24 secretion. The M2 macrophages also exhibited increased levels of Arg1 activity and reduced levels of IL-10 expression, relative to macrophages derived from control mice. However, when evaluating the expression of markers associated with classically activated (M1) macrophages, namely inducible nitric oxide synthase and IL-12, it was observed that levels of M1 markers in the interstitial macrophages from asthmatic mice did not differ significantly to those in controls. Collectively, these data suggest that lung interstitial macrophages undergo a phenotypic switch from a regulatory macrophage phenotype under normal conditions to an alternative activation state in OVA-induced asthmatic mice.
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影响因子：
4.4
作者：
Gerber, JS;Mosser, DM
通讯作者：
Mosser, DM
影响因子：
15.9
作者：
Bedoret, Denis;Wallemacq, Hugues;Bureau, Fabrice
通讯作者：
Bureau, Fabrice
影响因子：
158.5
作者：
Chupp, Geoffrey L.;Lee, Chun Geun;Elias, Jack A.
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Elias, Jack A.
影响因子：
3
作者：
Ford AQ;Dasgupta P;Mikhailenko I;Smith EM;Noben-Trauth N;Keegan AD
通讯作者：
Keegan AD
影响因子：
3.1
作者：
Martinez, Fernando Oneissi;Sica, Antonio;Locati, Massimo
通讯作者：
Locati, Massimo