Surface and transmission ultrastructural characteristics of desquamative interstitial pneumonitis.
A prospective study of eight patients with desquamative interstitial pneumonitis was performed, correlating surface ultrastructure as elucidated by scanning electron microscopy, transmission electron microscopy, viral cultures of fresh sterile lung tissue obtained at thoracotomy, and immunomicroscopy. The hypothesis that environmental pollutants may act as sensitizing agents to induce macrophage migration was pursued using high resolution elemental analysis to obtain a profile of the inorganic content of phagolysosomes in the free alveolar cell population. Four surface ultrastructural changes were observed: mild alveolar septal thickening, an apparent decrease in the number of pores of Kohn, alteration of the predominant alveolar lining population from membranous to granular pneumonocytes, and prominent intra-alveolar collections of cells with broad based ruffled projections and pseudopodia representing a macrophage population. Transmission electron microscopy corroborated these observations. Individual pneumonocyte degeneration manifested as cytoplasmic dissolution, mitochondrial swelling, chromatin disruption, and loss of lamellar bodies and endoplasmic reticulum was identified; occasionally degenerating granular pneumonocytes were displaced into the alveolar space by a supraseptal bulla containing fibrin and extracellular fluid. Viruses were not identified by ultrastructural or tissue culture techniques. High resolution elemental analysis of individual phagolysosome contents failed to reveal the presence of heavy metals or other inorganic compounds. Immune complexes were not identified by immunofluorescence microscopy. However, alveolar transeptal macrophage migration was observed by transmission electron microscopy. These observations suggest that desquamative interstitial pneumonitis represents a disease in which cellular, rather than humoral, immune processes predominate. Other nonspecific cellular immune responses under the influence of various lymphokines may be responsible for the observed morphologic alterations.
D003094:Collagen; D003593:Cytoplasm / Q000648:ultrastructure; D003594:Cytoplasmic Granules / Q000648:ultrastructure; D006801:Humans; D008168:Lung / Q000648:ultrastructure*; D008247:Lysosomes / Q000032:analysis; D008264:Macrophages / Q000502:physiology; D009940:Organoids / Q000648:ultrastructure; D011650:Pulmonary Alveoli / Q000648:ultrastructure*; D011658:Pulmonary Fibrosis / Q000473:pathology*
D003094:Collagen