Autophagy has been involved in the pathogenesis of various lung diseases. However, it is not yet known whether autophagy plays a role in hypersensitivity pneumonitis (HP). HP is an interstitial lung disease resulting from exposure to a wide variety of antigens that provoke an exaggerated immune response in susceptible individuals. The aim of this study was to explore the localization of autophagy key proteins in lungs from HP patients and controls by immunohistochemistry and analyze their expression levels by immunoblot. Macrophages and epithelial cells were strongly positive for the autophagosome biomarker LC3B (microtubule-associated protein light chain 3 beta) in HP lungs compared with controls. A similar pattern was found for the autophagy receptor p62 and the enzyme ATG4B. Unexpectedly, nuclear p62 signal was also noticed in macrophages from HP lungs. Regarding ATG5 and ATG7 localization, we observed positive staining in neutrophils, vascular smooth muscle cells, and endothelial cells. Our findings provide for the first time evidence that proteins from the autophagy machinery are highly expressed in the lungs of HP patients and describe the specific cellular and subcellular localization of LC3B, p62, ATG4B, ATG5, and ATG7 in HP lungs:

自噬已参与各种肺部疾病的发病机理。但是，尚不清楚自噬是否在超敏性肺炎（HP）中起作用。HP是一种间质性肺病，是由于接触多种抗原引起的，这些抗原在易感人群中引起过度的免疫反应。这项研究的目的是通过免疫组织化学探索HP患者和对照肺中自噬关键蛋白的定位，并通过免疫印迹分析其表达水平。与对照组相比，巨噬细胞和上皮细胞在HP肺中的自噬生物标志物LC3B（微管相关蛋白轻链3 beta）强烈阳性。对于自噬受体p62和酶ATG4B也发现了类似的模式。不料，在HP肺巨噬细胞中也发现了p62核信号。关于ATG5和ATG7的定位，我们观察到中性粒细胞，血管平滑肌细胞和内皮细胞中的阳性染色。我们的发现首次为自噬机制的蛋白质在HP患者的肺中高表达提供了证据，并描述了HP肺中LC3B，p62，ATG4B，ATG5和ATG7的特定细胞和亚细胞定位：