Disruption in the balance between apolipoprotein A-I and mast cell chymase in chronic hypersensitivity pneumonitis.
Disruption in the balance between apolipoprotein A-I and mast cell chymase in chronic hypersensitivity pneumonitis.
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DOI：
10.1002/iid3.355
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发表时间：
2020-12
期刊：
影响因子：
--
通讯作者：
Miyazaki Y
中科院分区：
文献类型：
--
作者：
Inoue Y;Okamoto T;Honda T;Nukui Y;Akashi T;Takemura T;Tozuka M;Miyazaki Y
载脂蛋白A-I（apoA-I）在特发性肺纤维化中具有抗纤维化作用。尽管肺纤维化与过敏性肺炎（HP）患者的不良预后相关，但关于apoA-I在HP发病机制中的作用知之甚少。采用双向电泳、免疫印迹和酶联免疫吸附试验对急性和慢性HP患者支气管肺泡灌洗液（BALF）中的apoA-I进行鉴定和定量。为了研究apoA-I的降解，将apoA-I与BALF孵育。此外，检测了apoA-I在TGF-β1诱导的A549细胞上皮-间质转化中的作用。与急性HP（n = 31）相比，慢性HP（n = 56）中BALF中的apoA-I浓度显著较低。慢性HP肺组织中apoA-I的表达水平也较低。HP患者的BALF可降解ApoA-I。慢性HP患者肺泡实质中糜蛋白酶阳性肥大细胞数量与BALF中apoA-I水平呈负相关。在使用A549细胞的体外实验中，未处理的apoA-I抑制TGF-β1诱导的上皮-间充质转化，尽管在糜酶处理的apoA-I中未观察到这种趋势。apoA-I的降低与慢性HP肺纤维化的发病机制相关，肥大细胞糜酶减弱了apoA-I对肺纤维化的保护作用。此外，apoA-I可能是与HP肺纤维化相关的关键分子。载脂蛋白A-I（apoA-I）的降低与慢性过敏性肺炎（HP）的肺纤维化发病机制相关，肥大细胞糜酶减弱了apoA-I对肺纤维化的保护作用。此外，apoA-I可能是与HP肺纤维化相关的关键分子。
Apolipoprotein A‐I (apoA‐I) has an antifibrotic effect in idiopathic pulmonary fibrosis. Although pulmonary fibrosis is associated with poor prognosis of patients with hypersensitivity pneumonitis (HP), little is known regarding the role of apoA‐I in the pathogenesis of HP. Two‐dimensional electrophoresis, immunoblotting, and enzyme‐linked immunosorbent assays were performed for the identification and quantification of apoA‐I in bronchoalveolar lavage fluid (BALF) from patients with acute and chronic HP. To investigate the degradation of apoA‐I, apoA‐I was incubated with BALF. Moreover, the role of apoA‐I in TGF‐β1‐induced epithelial–mesenchymal transition of A549 cells was examined. The concentration of apoA‐I in the BALF was significantly lower in chronic HP (n = 56) compared with acute HP (n = 31). The expression level of apoA‐I was also low in the lung tissues of chronic HP. ApoA‐I was degraded by BALF from HP patients. The number of chymase‐positive mast cells in the alveolar parenchyma was inversely correlated with apoA‐I levels in the BALF of chronic HP patients. In vitro experiment using A549 cells, untreated apoA‐I inhibited TGF‐β1‐induced epithelial–mesenchymal transition, although this trend was not observed in the chymase‐treated apoA‐I. A decrease of apoA‐I was associated with the pathogenesis of chronic HP in terms of pulmonary fibrosis and mast cell chymase attenuated the protective effect of apoA‐I against pulmonary fibrosis. Furthermore, apoA‐I could be a crucial molecule associated with lung fibrogenesis of HP. A decrease of apolipoprotein A‐I (apoA‐I) was associated with the pathogenesis of chronic hypersensitivity pneumonitis (HP) in terms of pulmonary fibrosis and mast cell chymase attenuated the protective effect of apoA‐I against pulmonary fibrosis. Furthermore, apoA‐I could be a crucial molecule associated with lung fibrogenesis of HP.
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影响因子：
6.4
作者：
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通讯作者：
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作者：
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作者：
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影响因子：
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作者：
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