In this paper, problems on the pathogenesis of various pulmonary granulomas and alveolitis are reviewed.
1. Diffuse histiocytic reaction due to atypical mycobacteria.
A few cases of mycobacteriosis demonstrated diffuse histiocytic reaction with abundant intracellular acid-fast bacilli without caseous necrosis. Three possibilities might be consid ered for this peculiar lesion: (1) Mycobacteria in specific serotype may cause such lesion, (2) Suppressed immunological, especially cell-mediated reaction, may play an important role, as many simillar cases were reported in PPD negative children. (3) Specific intracel lular situation of the mycobacteria may result in the reaction: clear halo between the phagosomal membrane and the engulfed mycobacteria, which is also seen in leproma cells electronmicroscopically, may inhibit transmission of antigenic information to the cell.
2. Sarcoidosis, berylliosis and extrincic allergic alveolitis.
Epithelioid cell granulomas in sarcoidosis are presumed to develop by mitosis of single epithelioid cell which appeared in lymphocytic infiltration, not by gathering of many infiltrated precursor cells. Alveolitis in sarcoidosis is found extensively in the lung which show cotton-like shadow on chest X-ray films, accompanying dystelectasis in granulomatous area. Both of granuloma and alveolitis represent immunologic reactions to an unknown agent, which may be enhanced by adjuvant activities of Propioni-bacterium cultured in a high percentage in sarcoidosis lymph nodes.
In berylliosis, acute interstitial pneumonia, alveolitis, or chronic granulomatous change appears following inhalation of soluble or insoluble beryllium respectively, in conjugation with serum albumin.
In extrinsic allergic alveolitis, both of diffuse alveolitis and typical or immature epithe lioid cell granuloma with slight bronchiolitis are the characteristic features of the disease. The extent of each lesion may depend upon wheather the antigen is water-soluble or in particulate form.
3. Eosinophilic granuloma (EG), HandSchullerChristian‘disease (HSC) and Letterer Siwe’ disease (LS).
EG, HSC and LS had been included in a disease entity, Histiocytosis-X (HX), by Lichterstein in 1953. However, histopathological features of the three diseases were found to differ markedly, upon the observation of autopsy and biopsy cases collected from many institutions in Japan. Early change of pulmonary EG seemed to appear in the bronchiolar walls, spread in the wall of peripheral airways, replacing them by granulomatous changes and resulted in cystic dilatation of airway lumens. Otherwise, nodular lesions are formed based on the alveolar walls, with intraalveolar changes.
Characteristic histologic feature of HSC are foamy Langerhans' (L) cell infiltration with marked fibrosis, usually limited to the interstitial connective tissue of various organs. Intra-lymphangic or intra-sinus accumulation of L cell were found in the lobular septum of lung or of the lymphnodes, respectively.
In LS, diffuse infiltration of L cells and mononuclear cells were found in the alveolar walls of the lung, lymphatic tissue of the lymph nodes, thymus, white pulp in the spleen, tonsils, intestinal lymphatic tissues and liver sinusoids. Intra-vascular localisation was noted in the lung, indicating hemic spread of the L-cells.
It is better to diagnose using each name of the disease, or to diagnose as HX (EG), HX (HSC) and HX (LS).
4. Idiopathic interstitial fibrosis of the lung (IIF)

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