The ultrastructural changes occurring in the alveolar area, especially in the epithelial tissue, of lung diseases were follwed by scanning electron microscopy and transmisson electron microscopy.
(1) Alveolar epithelial cells in the healthy lung.
Interalveolar septa in the healty lung were covered continuously with two kinds of epithelial cells; type A epithelial cell and type B epithelial cell. Phylogentic and ontogenetic studies showed that both epithelial cells closely related with each other. Type A cell is so flat in its shape as be convenient gas exchange, while type B cell secrets surfactant and prevents the alveolus for atelectasis.
(2) Alveolar lining layer.
Phospholipid staining suggested that phospholipid in the alveolar lining layer was derived from lamellar inclusion bodies type B cells in the manner of merocrine secretion and microapocrine secretion. The mucopolysaccharide layer stained by Groniowski's method belongs to the cell coat of epithelial cells.
(3) Interstitial pneumonia and pulmonary fibrosis.
Type B alveolar epithelial cells are resistant to injury, and to replace the denuded regions from which type A epithelial cells have been detached. Therefore, type B cells are considered to play a role as a reserve source for epithelial cells in the alveolar regions, and to form the adenomatous hyperplasia of the alveolar epithelial cells.
(4) Desquamative interstitial pneumonia.
Electron microspic examination suggested that free cells in the alveolar spaces were predominantly mesenchymal, while a few were type B epithelial cells.
(5) Pulmonary alveolar proteinosis.
The proteinaceous materials which fill the alveolar spaces are mostly derived from disintegrated mesenchymal cells of the interalveolar septa. The lesion consisted of the area of desquamation and sloughing of these cells and the area of deposition of disintegrated cells.
(6) Pulmonary sclerosing hemangioma.
Blood-filled spaces in the tumor were lined with epithelial cells which closely resembled type B cells. In many cases, these cells tended to grow into connective tissus to form sheets or clusters of cells.
(7) Urethane-induced pulmonary adenoma.
The resemblance in the fine structure of tumor cells to that of type B cells provided strong evidence that the type B cells proliferated and formed the pulmonary adenoma.
(8) Human lung cancer.
Osmiophilic lamellar inclusion bodies similar to those of type B cells were occasionally found in alveolar cell carcinomas and peripheral adenocarcinomas. The presence of these inclusion bodies lends support to the suggestion that these tumors have their origin in the alveolar epithelium.

View full abstract

Clinical and pathological examinations were conducted on a case of desquamative interstitial pneumonia.
A 30 year-old male was admitted to hospital, complaining of dyspnea, and showing an acinar pattern on his chest X-ray. The sputum revealed collections of alveolar macrophages, some of which were foamy. An open lung biopsy was performed in order to obtain a definite diagnosis.
Microscopically large mononuclear cells filled the alveolar spaces, and no hyaline membrane was present. Thickening of the alveolar walls with lymphocyte infiltration was found partially.
Electron-microscopically intraalveolar cells showed the features of alveolar macrophages. The basement membrane was intact.

View full abstract

The purpose of the study was to investigate the pathological changes in the respiratory organs in 9 autopsy cases to elucidate the histogenesis of the disease.
The initial lesions occurred in any site of the respiratory tract from the nose to the lung and all cases showed a widespread ulcerative granulomatous inflammation. The histopathological findings were a granulomatous inflammation resembling tuberculosis, but a non-specific inflammation and necrotizing or granulomatous vasculitis were also noted in various degrees. Lesions showed a progressive and destructive tendency. Saddle nose occurred in 5 cases of which 2 had exophthalmos. In 6 cases, severe pulmonary lesions with cavity formation in various sizes were observed, characterized by granulomatous inflammation, angitis and alveolitis. Of the remaining 3 cases, 2 showed small foci of angitis and 1 no remarkable changes. Small granulomata or fresh exudative lesions were found in the bronchial wall and the peripheral air passage. In the vicinity of these initial lesions, vascular lesions were minimal or uncommon. These findings suggest that the initial pulmonary lesions might be induced by an air-borne antigen.
Vascular lesions in the respiratory tract were found most frequently in and around the granulomatous area with a close relation to granulomatous inflammation. Therefore, vascular lesions assumedly followed the preceding granulomatous inflammation in the respiratory tract, with a counter relation between granulomata and angitis occurring in the other organs.
From these observations, it may be reasonable to consider that Wegener's granulomatosis might be initiated as a progressive granulomatous inflammation of an unknown etiology of hypersensitivity in the respiratory tract. The involvement of blood vessels in the other organs and glomeruli appears most probably to follow the development of hypersensitivity generalized in the whole body.

View full abstract

A 31-year-old woman, who had twice histories of spontaneous abortion, showed abnormal shadow on chest roentogenogram, multiple nodular shadows on both lungs.
It was suspected to be metastasis of chorionepithelioma malignum or other metastic pulmonary carcinomas, but could not be found firm evidence for diagnosis. Six months later open lung biopsy was performed and it disclosed that the nodules were tuberculous granuloma.

View full abstract