PubMed Health⌕ Search

Biomedical subjects

O Kawanami

Publications and source records attributed to O Kawanami.

At least 73 records · Page 4Linked to original sources
PubMed1983

Hypersensitivity pneumonitis in man. Light- and electron-microscopic studies of 18 lung biopsies.

Light- and electron-microscopic changes produced by hypersensitivity pneumonitis were analyzed in open lung biopsies taken from 18 patients with chronic forms of the disease. The main changes observed were: alveolitis (both luminal and mural), granulomas, intraalveolar buds, and interstitial fibrosis. The cells infiltrating the alveolar walls were mainly lymphocytes. Occasionally these lymphocytes presented irregularities in the contours of the nuclear membranes and resembled Sézary cells. In one patient, a few lymphocytes were found that resembled "hand-mirror" cells. Intraalveolar macrophages often had a foamy appearance. Granulomas, present in two-thirds of the patients, differed in several respects from those in sarcoidosis: they were smaller, more loosely arranged, and poorly limited; they had a higher content of lymphocytes; and they were located more frequently in alveolar tissue than in the vicinity of bronchioles and vessels. Intraalveolar buds, also present in about two thirds of the patients, were composed mainly of fibroblasts, myofibroblasts, and macrophages in a loose connective tissue that was rich in proteoglycan material. Capillaries and epithelial cells were rarely seen in buds. Alveolar buds appear to develop by a process of disruption of the epithelial lining layer, due to alveolitis, followed by intraalveolar exudation and by subsequent intraalveolar migration of connective tissue cells interacting with macrophages. Severe fibrotic and alveolar epithelial changes were observed in four patients; milder changes were frequent in most other patients. It is concluded that hypersensitivity pneumonitis usually has distinctive morphologic features; these may help to distinguish the resultant pulmonary fibrosis from that due to other causes.

Adult↗
PubMed1982

Anthracycline-induced histamine release from rat mast cells.

Comparisons were made of the ability of doxorubicin, daunorubicin, rubidazone and aclacinomycin A to release histamine from rat peritoneal mast cells. Preliminary in vitro experiments indicated that doxorubicin (10(-6) to 2.5 X 10(-4) M), in contrast to compound 48/80 and the calcium ionophore A23187, did not produce significant release under any condition tested when purified or unpurified rat mast cells were used. In in vitro experiments, released histamine was measured in the cell-free supernatant of peritoneal fluid of rats after intraperitoneal injection of the agents. The time course of doxorubicin-induced histamine release from the peritoneum was rapid, with maximal release occurring within 4 to 6 min. Dose-response curves of the 4 agents over the range 10(-5) to 3.3 X 10(-3) M revealed that all caused histamine release, with 10(-3) M concentrations of each causing maximal release of comparable magnitude to that produced by 9.5 X 10(-6) M A23187. Treated mast cells recovered from the peritoneal cavity showed degranulation and vacuolization when examined by electron microscopy. Increased vascular permeability by the Evans-blue test was also noted with all 4 agents, and zones were of comparable size after injection of the highest concentration of each agent. The results indicate that in vivo, doxorubicin, daunorubicin, rubidazone and aclacinomycin A cause a rapid release of histamine from rat mast cells and an increase in vascular permeability in rat sin. There also appeared to be a reasonable correlation between the blueing reaction and histamine release in the peritoneal cavity in that the doses that did not cause skin blueing also failed to cause histamine release. The lack of histamine release by doxorubicin from mast cell preparations in vitro suggests that alterations to the doxorubicin molecule or the presence of other critical substances may be necessary for this activity to commence.

Aclarubicin↗
PubMed1982

Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure.

After intratracheal injection of short chrysotile asbestos fibres in guinea-pigs an intense neutrophil alveolitis was observed within three days. Evaluation by bronchoalveolar lavage of the inflammatory and immune effector cells producing the alveolitis by three days showed an increased proportion of polymorphonuclear leucocytes, which comprised 21% +/- 3% of the total leucocytes compared with 9% +/- 2% for the controls (p less than 0.05), persisting for at least six weeks (after which time the polymorphonuclear leucocytes comprised 28% +/- 2% compared with 7% +/- 1% for the controls: p less than 0.05). One mechanism by which asbestos fibres may cause polymorphonuclear leucocytes to be attracted to the alveolar structures is by induced release of neutrophil chemotactic factor by alveolar macrophages. When exposed in vitro to short or intermediate chrysotile fibres or amosite or crocidolite fibres guinea-pig alveolar macrophages released appreciable amounts of neutrophil chemotactic factor. The release of this chemotactic factor was augmented when the asbestos fibres had been previously exposed to normal serum. The chemotactic factor was lipid soluble, and was similar to the neutrophil chemotactic factor spontaneously released by alveolar macrophages recovered from guinea-pigs exposed in vivo to short chrysotile fibres. These observations suggest that alveolar macrophages may play an important part in the early stages of asbestosis by modulating the migration of neutrophils to the lung.

Animals↗
PubMed1982

Structure of alveolar epithelial cells in patients with fibrotic lung disorders.

Ultrastructural studies were made of the types of alveolar epithelial cells in fibrotic lungs from 34 patients, including 20 with idiopathic pulmonary fibrosis, five with collagen-vascular diseases, six with sarcoidosis, one with lymphangioleiomyomatosis, one with histiocytosis X, and one with chronic eosinophilic pneumonia. In 28 patients, proliferation of type II alveolar epithelial cells was recognized on the basis of lamellar bodies in the cytoplasm, microvilli in the luminal surface, focal microfoldings of the basal plasma membrane, close interaction with underlying mesenchymal cells, and unilayered arrangement. Two types of cuboidal epithelial cells were recognized and were considered to be derived from bronchiolar basal cells (type A cuboidal cells) and from cuboidal cells in respiratory bronchioles (type B cuboidal cells). Type A cuboidal cells frequently contained large numbers of cytoskeletal filaments, and their basal plasma membranes possessed hemidesmosomes in close association with anchoring fibrils. Type B cells lacked hemidesmosomes and anchoring fibrils, Proliferation of either or both types of cuboidal cells was found in 30 patients. In 10 patients (average degree of fibrosis = 3.5 on a scale of 0 to +4), the proliferation involved type A cells; in 10 other patients (average degree of fibrosis = 2.5), type B cells in nine patients (average degree of fibrosis = 3.4), both type A and type B cells; in one patient cuboidal cells were identified only by light microscopy. In 17 patients, proliferating cuboidal cells formed foci of epithelial pseudostratification. Type II alveolar epithelial cells did not participate in the process of multilayering. Thus, type II alveolar epithelial cells and two types of cuboidal epithelial cells are sources of epithelial renewal in damaged alveoli in fibrotic lungs. Type II cells proliferate mainly in areas of less severe degrees of fibrosis; cuboidal cells become the main source of epithelial renewal in areas of very severe lung damage.

Biopsy↗
PubMed1981

Hereditary emphysema in the tight-skin (Tsk/+) mouse.

The tight-skin (Tsk/+) mouse represents an autosomal dominant mutation characterized by increased thoracic size, large lungs, and a variety of abnormalities of loose subcutaneous connective tissue, cartilage, tendon, and bone. Because an increase in the size of the lung and thorax may result from destruction of alveolar walls and a loss of elastic recoil of the lung, the present study was undertaken to determine if the Tsk/+ mouse exhibits morphologic and physiologic characteristics of emphysema. In contrast to the lungs of normal mice, examination of the lungs of Tsk/+ mice by light and scanning electron microscopy revealed generalized enlargement of air spaces with numerous subpleural cysts and scattered bullae. In addition, many alveolar walls were either markedly thinned or broken and there was an increase in the number and size of the pores of Kohn. Consistent with these morphologic observations, the lungs of the Tsk/+ mice also exhibited physiologic characteristics consistent with emphysema. Compared to the lungs of normal mice, the lungs of Tsk/+ mice had a markedly increased total lung capacity of (1.8 +/- 0.1 ml versus 3.3 +/- 0.1 ml, p less than 0.001); compliance (0.077 +/- 0.006 ml/cm H2O versus 0.345 +/- 0.025 ml/cm H2O, p less than 0.001), and specific compliance (4.23 +/- 0.34% TLC/cm H2O versus 10.64 +/- 1.01% TLC/cm H2O, p less than 0.001). These findings suggested that the Tsk/+ mouse is a genetically determined model of emphysema that may be useful in determining the pathogenesis of destructive lung disease.

Animals↗
PubMed1981

Pulmonary Langerhans' cells in patients with fibrotic lung disorders.

Langerhans' cells were found in lung biopsies in one of nine control patients and in 20 of 160 patients with fibrotic lung disorders, including 13 of 56 patients with idiopathic pulmonary fibrosis, two of nine patients with collagen vascular diseases, two of seven patients with hypersensitivity pneumonitis, and each of three patients with end stage fibrosis of uncertain cause. Langerhans' cells were not found in any of the 41 patients with sarcoidosis, the 35 patients with interstitial lung diseases associated with inhalation of inorganic dusts, the seven patients with pulmonary lymphangioleiomyomatosis, or the two patients with chronic eosinophilic pneumonia. In the control patient, Langerhans' cells were found between epithelial cells in bronchioles. In patients with fibrotic lung disorders, Langerhans' cells were found in the epithelial layer of bronchioles and alveoli containing proliferating epithelial cells, i.e., either cuboidal epithelial cells of bronchiolar origin or type II alveolar epithelial cells. Severe fibrosis or squamous metaplasia were not prerequisites for the presence of Langerhans' cells. The motility of Langerhans' cells apparently was restricted, as they were not found in the air spaces in any of the biopsies, and they were not recovered from bronchoalveolar lavage fluid of any of the 97 patients studied, even though some of these patients had relatively numerous Langerhans' cells in lung biopsies. These observations are in sharp contrast to those in pulmonary histiocytosis X, in which histiocytosis X cells (HX cells) occur in granulomas, in alveolar interstitium, and between epithelial cells of the lower respiratory system. HX cells also migrate into air spaces, as shown by their occurrence in bronchoalveolar lavage fluid. The HX bodies in HX cells are morphologically similar to Langerhans' cell granules, but are more numerous and pleomorphic. HX cells are considered to be reactive or activated Langerhans' cells.

Alveolitis, Extrinsic Allergic↗
PubMed1980

Maintenance of granuloma formation in pulmonary sarcoidosis by T lymphocytes within the lung.

Pulmonary granulomata of sarcoidosis are composed primarily of mononuclear phagocytic cells that are probably derived from blood monocytes. To evaluate the concept that recruitment of blood monocytes to the sarcoid lung is mediated by chemoattractants produced by immune effector cells within the lung, we obtained mononuclear cells from lung and blood of six patients with active pulmonary sarcoidosis, six normal subjects, and six patients with active idiopathic pulmonary fibrosis and studied their ability to secrete a chemotactic factor for monocytes. Lung T lymphocytes from all sarcoidosis patients, but not from normal subjects or patients with idiopathic pulmonary fibrosis, spontaneously secreted such a mediator. Lung T lymphocytes from patients with sarcoidosis secreted more monocyte chemotactic factor than did blood T lymphocytes from the same patients. The accumulation of monocytes in the lung in patients with pulmonary sarcoidosis may be mediated by local production of monocyte chemotactic factor by lung T lymphocytes.

Adult↗
PubMed1980

Histologic and ultrastructural features of normal human parietal pericardium.

Morphologic studies of normal anterior parietal pericardium from seven patients revealed this tissue to be composed of three layers: (1) the serosa, consisting of a surface layer of mesothelial cells and a narrow submesothelial space, (2) the fibrosa, containing variously oriented layers of collagen fibrils and small elastic fibers, and (3) the epipericardial connective tissue layer, containing mainly large coarse bundles of collagen and forming part of the pericardiosternal ligament. Scanning electron microscopic examination is most useful for study of the surface features of pericardial mesothelial cells, which have single cilia and are covered with microvilli. The latter bear friction and increase the surface area for fluid transport. Junctional complexes between adjacent mesothelial cells consist of desmosomes, which reinforce intercellular adhesion and zonulae occludentes, which form permeability barriers. Actin-like filaments (50 A in diameter) are present in microvilli and in immediately subjacent regions of the cells; these filaments mediate changes in cell shape. Intermediate filaments (100 A in diameter) are associated with desmosomes and form bundles in the perinuclear regions; these filaments provide structural support to the cytoplasm.

Adolescent↗
PubMed1980

Subplasmalemmal linear densities in cells of the mononuclear phagocyte system in lung.

The presence of subplasmalemmal linear densities in cells of the mononuclear phagocyte system was investigated in pulmonary biopsies from 33 patients with fibrotic lung disorders. Subplasmalemmal linear densities, consisting of a thin layer of electron-dense material immediately subjacent to the inner leaflet of the plasma membrane, were found in 30 of the 33 patients, including each of 6 patients with pulmonary sarcoidosis, 18 of 19 patients with idiopathic pulmonary fibrosis, 4 of 5 patients with collagen-vascular diseases, 1 patient with pulmonary lymphangioleiomyomatosis, and 1 patient with marked interstitial pulmonary fibrosis associated with squamous cell carcinoma of the lung. Subplasmalemmal linear densities were found in epithelioid cells, macrophages, and giant cells in granulomas in the 6 patients with sarcoidosis and in alveolar macrophages in 4 of these patients. In patients with other fibrotic lung disorders, subplasmalemmal linear densities were limited in distribution to interstitial and alveolar macrophages. In all patients with sarcoidosis some of the subplasmalemmal linear densities of adjacent mononuclear phagocytes, particularly of those in granulomas, were paired and formed specialized intercellular junctions. Such junctions also were observed in macrophages in 10 of the patients with other fibrotic lung disorders. The junctions formed by subplasmalemmal linear densities differed from other types of junctional structures. Subplasmalemmal linear densities appear to function in 1) the binding of action filalar junctions, which may contribute to the immobilization of mononuclear phagocytes in granulomas and alveolar lumens.

Actinin↗
PubMed1979

Anchoring fibrils in the normal canine respiratory system.

Electron microscopic study of the normal canine respiratory tree disclosed the presence of anchoring fibrils, a distinct class of fibrils of extracellular connective tissue, in association with the following types of cells: (1) basal cells and special type cells of trachea and bronchi; (2) ciliated cells and basal cells of bronchioles; (3) ductal cells, secretory cells, and myoepithelial cells of tracheobronchial glands. Anchoring fibrils in the normal respiratory system measured up to 6,000 A in length and from 170 to 400 A in thickness, and had a banding pattern that differed from that of collagen fibrils and connective tissue microfibrils. They formed arcs, the ends of which inserted into the basal lamina underlying the basal portions of the cells, often in the vicinity of hemidesmosomes. Anchoring fibrils decreased in number and size in the more distal portions of the respiratory tree, and were not found in alveolar septums. Anchoring fibrils in lung appeared similar to those described in other organs, but were often small and inconspicuous. The function of these structures is to reinforce the attachment of the epithelial basal lamina to the underlying connective tissues.

Animals↗
PubMed1979

Nuclear inclusions in alveolar epithelium of patients with fibrotic lung disorders.

Ultrastructural study of pulmonary biopsy specimens from patients with fibrotic lung disease disclosed the presence of nuclear inclusions in 1% or less of cuboidal alveolar epithelial cells in 9 of 19 patients, including 6 of 12 patients with idiopathic pulmonary fibrosis, 2 of 3 patients with collagen-vascular disease, and 1 of 3 patients with sarcoidosis. Nuclear inclusions were not observed by ultrastructural study in 5 control patients. The inclusions consisted of masses or aggregates of tubules which probably were derived from the inner nuclear membranes. These tubules were smooth-walled, showed branchings and bifurcations, were composed of single trilaminar membranes, usually had a clear content, and ranged from 500 to 1000 A in diameter. They resembled nuclear tubules which occur in other cell types under conditions of rapid growth or specific hormonal stimulation. Statistically significant differences between the groups of patients with and without nuclear inclusions in cuboidal alveolar epithelial cells were not found with respect to smoking history, degree of fibrosis in the lung biopsy specimen, or the degree of pulmonary physiologic impairment. However, the average age of the patients having nuclear inclusions was significantly greater than that of patients not having nuclear inclusions. In addition, the frequency of indentations in the nuclei of cuboidal alveolar epithelial cells was greater in patients with nuclear inclusions than in patients without nuclear inclusions. Highly significant correlations were observed between the presence of nuclear inclusions and the presence of a) anchoring fibrils and hemidesmosomes along the basal surfaces of alveolar epithelial cells and b) multilayering of the alveolar epithelium.

Aging↗