Janin A, Torpier G, Courtin P, Capron M, Prin L, Tonnel A B, Hatron P Y, Gosselin B
Department of Pathology C, Hôpital Calmette, Lille, France.
Thorax. 1993 Jan;48(1):57-62. doi: 10.1136/thx.48.1.57.
The objective was to characterise the process and consequences of eosinophil activation and lysis in patients with chronic eosinophilic pneumonia and to compare them with those in patients with eosinophil pulmonary infiltrates from other causes.
Cells from bronchoalveolar lavage fluid of four patients with chronic eosinophilic pneumonia and four patients with eosinophilic infiltrates associated with Sjögren's syndrome, drug hypersensitivity pneumonia, postradiotherapy fibrosis, and pulmonary disease associated with graft versus host disease were studied ultrastructurally and with immunogold labelled antibodies directed against eosinophil proteins: major basic protein, eosinophil cationic protein, and Charcot-Leyden crystal protein. The concentration of eosinophil cationic protein was also measured in bronchoalveolar fluid.
In the four patients with chronic eosinophilic pneumonia, ultrastructural studies demonstrated numerous lysed eosinophils. Further, three released eosinophil proteins were detected in distinct cytoplasmic structures in alveolar macrophages. These features were not found in the four patients with eosinophilic pulmonary infiltrates from other causes.
Eosinophils in chronic eosinophilic pneumonia show signs of activation with release of eosinophil proteins. The appearance of three of these eosinophil proteins in different macrophage compartments suggests that macrophage uptake, with or without intracellular transport of released eosinophil proteins, involves separate mechanisms. This interaction does not lead to macrophage lysis, however, and one or more of these eosinophil proteins might directly affect macrophage function.
目的是描述慢性嗜酸性粒细胞性肺炎患者嗜酸性粒细胞活化和溶解的过程及后果,并将其与其他原因引起的嗜酸性粒细胞肺浸润患者的情况进行比较。
对4例慢性嗜酸性粒细胞性肺炎患者以及4例与干燥综合征、药物性过敏性肺炎、放疗后纤维化和移植物抗宿主病相关的嗜酸性粒细胞浸润患者的支气管肺泡灌洗液细胞进行超微结构研究,并使用针对嗜酸性粒细胞蛋白(主要碱性蛋白、嗜酸性粒细胞阳离子蛋白和夏科-莱登结晶蛋白)的免疫金标记抗体进行研究。还测量了支气管肺泡液中嗜酸性粒细胞阳离子蛋白的浓度。
在4例慢性嗜酸性粒细胞性肺炎患者中,超微结构研究显示有大量溶解的嗜酸性粒细胞。此外,在肺泡巨噬细胞的不同细胞质结构中检测到三种释放的嗜酸性粒细胞蛋白。在其他原因引起的嗜酸性粒细胞肺浸润的4例患者中未发现这些特征。
慢性嗜酸性粒细胞性肺炎中的嗜酸性粒细胞表现出活化迹象并释放嗜酸性粒细胞蛋白。这三种嗜酸性粒细胞蛋白在不同巨噬细胞区室中的出现表明,巨噬细胞摄取释放的嗜酸性粒细胞蛋白,无论有无细胞内转运,都涉及不同的机制。然而,这种相互作用不会导致巨噬细胞溶解,并且这些嗜酸性粒细胞蛋白中的一种或多种可能直接影响巨噬细胞功能。