Robert E. Brooks

Lung alveolar cell cytosomes: A consideration of their significance

SummaryAn ultrastructural comparison of mammalian, reptilian, and amphibian lung alveolar cells, and avian lung atrial cells reveals that morphologically similar cytoplasmic bodies (cytosomes) occur in these cells. The cytosomes, which appear generally as osmiophilic, lamellae-containing, membrane-bound, round bodies 0.3 to 0.5 μ in diameter, are also similar to bodies occurring in epithelial cells of both physoclistous and physostomatous swimbladders of fishes. Because the function of both lung alveolar and swimbladder epithelial cells is gas-handling, the possibility is raised that the morphologically similar lamellae-containing bodies of these vertebrate cells are functionally identical. One function, suggested by other investigators, is that, in mammalian lungs, these bodies supply a surface-tension lowering material (surfactant). Because several assumptions concerning this proposed function remain unproved, an alternative proposal is speculatively explored. The suggestion is offered that cytosomes contain an antioxidant needed to protect alveolar and swimbladder cells against the toxic effects of the relatively high concentration of oxygen to which these cells are exposed.

Ultrastructure of the physostomatous swimbladder of rainbow trout (Salmo gairdneri)

SummaryRainbow trout swimbladder epithelium consists of non-ciliated and ciliated cells in the ratio of greater than 2∶1. Non-ciliated cells contain vesicles filled with a mucus-like material and similar material is found lining the surface of the swimbladder lumen. Morphological evidence for discharge of the vesicle contents was obtained. In addition, nonciliated cells contain osmiophilic lamellar bodies which resemble the cytosomes of lung alveolar cells of air-breathing vertebrates. The non-ciliated cells do not appear to be involved in a process of active gas secretion.

Kidney tubule basement membrane alterations in type II membranoproliferative glomerulonephritis.

Fourteen kidney biopsy specimens from nine patients with type II membranoproliferative glomerulonephritis (MPGN) were examined by electron microscopy for tubular basement membrane (TBM) alterations. In all biopsies, laminal densities, characteristic for type II MPGN, were present in the glomerular basement membranes. The TBM alterations observed included: 1) the presence of laminal, and/ or discrete, and/or aggregated densities; 2) focal thickening; 3) multilamination; and, 4) vesicular structures. Laminal densities occurred in 6 of the 9 cases examined. All biopsies had TBM densities representative of at least one of the three forms. The occurrence of electron densities in or near the TBM in type II MPGN may have diagnostic value. In those biopsies where tissue is insufficient for immunofluorescence microscopy and where glomeruli are not found on electron microscopy, an electron microscopic search for densities associated with TBMs would be warranted. Although TBM-associated densities are not pathognomonic for type II MPGN, the observation of such densities, especially laminal densities, would be useful in complementing light microscopic and clinical findings.

Mitosis of type B alveolar cells in the early hyperplastic response to Freund's adjuvant.

SummaryNumerous areas of granulomatous inflammation develop in the lungs of rabbits following the intravenous injection of Freund’s complete adjuvant (FCA). Within a few days after FCA injection, hyperplasia of type B (type I) alveolar cells is present on the surface of the septa in which an inflammatory reaction is developing. Mitosis of type B cells is detected 12 h after FCA injection and is common over the next 120 h. In addition, there are morphologic changes that are consistent with migration of these cells. The type B cells in mitosis extend across alveolar septa as well as along the alveolar surface. The extension of type B cells through alveolar septa is not limited to cells in mitosis, but is also observed in non-mitotic type B cells. Stimulation of mitosis and hyperplasia of type B cells is discussed in relation to the focal tissue injury and inflammatory response.