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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies of influenza virus infections have focused on the acute pathologic manifestations associated with the virus pneumonia; however, there is evidence suggestive of persistent pathologic processes with possible long-term consequences. Herein we have examined the long-term outcome of virus pneumonia in mice infected by aerosol inhalation of a sublethal dose of influenza A/PR8/34 virus. At 3, 5, 7, 9, 15, 30, 60, 90, 120 days, and a year thereafter, the lavageable lung cell populations and differential counts were quantitated. Consistent with previous studies we demonstrated an inflammatory cellular response during the acute phase of the infection. However, this inflammatory response did not completely resolve, the pulmonary leukocytosis remaining stable from Day 30 through a year after virus infection. For example, on Day 30, virus-infected lungs yielded 12.4 +/- 0.9 X 10(5) cells per lavage of which 15 +/- 3% were polymorphonuclear leukocytes, 18 +/- 4% were lymphocytes, and 67 +/- 5% were alveolar macrophages. In contrast, 7.2 +/- 0.5 X 10(5) cells per lavage were obtained from uninfected lungs of which more than 98% were alveolar macrophages. Histopathologic examination of virus-infected lungs showed an ongoing inflammatory response resulting in patchy mononuclear interstitial pneumonia, deposition of collagen in the affected areas, and marked hyperplasia of bronchial-associated lymphoid tissue. Infectious virus could not be recovered after Day 9. However, in contrast to loss of infectivity, viral antigen persisted at high concentrations in the lung. We conclude that influenza virus infection induced a long-term alveolitis that is associated with persistence of viral antigen. These data open the possibility that influenza virus infections may play a role in interstitial lung disease.
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PMID:Alveolitis induced by influenza virus. 662 51

The pathological lesions of bagassosis have been reproduced in guinea pigs given bagasse fibers along with low doses of actinomycete spores. In the early stages, interstitial infiltration with lymphocytes and macrophages as seen in humans was noted. Later, small interstitial bagasse granulomas composed of foreign body giant cells, fibroblasts, and lymphocytes developed, some of which had a laminated appearance. Lymph node changes consistent with an immunological reaction were observed. Actinomycetes alone showed occasional areas of pneumonitis and bagasse alone small granulomas consisting of foreign body giant cells and bagasse fibers. Finally, the combined effect of dust and actinomycetes produced interstitial fibrosis composed of thick reticulin fibers and occasional collagen fibers, which persisted to the end of the experiment. Bagasse alone and actinomycetes alone produced only thin reticulin fibers. It has been suggested that bagassosis is due to the synergistic action of bagasse fibers and Micropolyspora faeni and that in the pathogenesis of the syndrome an immunological component may be involved.
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PMID:Experimental bagassosis: role of infection. 688 91

This study examines the effect of irradiation on lung surfactant synthesis and secretion in mice. Animals were irradiated with 650, 1300, or 1950 rad and morphological and biochemical indices of surfactant system function were followed for 18 weeks. No changes were seen at 650 rad; the results at 1300 and 1950 rad were virtually identical. Increased amounts of alveolar surfactant phospholipid were measureable by 24-hours. This persisted for four weeks and returned to normal by 18 weeks. Tissue surfactant phospholipid was initially reduced, returned to normal by four weeks and was increased at 18 weeks. At 18 weeks there was increased incorporation of surfactant precursor and increased production of alveolar surfactant. These biochemical changes were reflected in morphologic alterations showing release of lamellar body contents into alveoli in the first week and an increase in lamellar bodies in type II pneumocytes by 18 weeks. Elevated tissue protein levels and morphologic evidence of increased collagen formation were also found at 18 weeks. These findings indicate effects of irradiation on the pulmonary surfactant system and have important implications for the pathogenesis and potential therapy of radiation pneumonitis.
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PMID:Sequential effects of irradiation on the pulmonary surfactant system. 689 8

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.
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PMID:Pulmonary Langerhans' cells in patients with fibrotic lung disorders. 697 Mar

Pulmonary function studies were done serially in 23 children 7 to 18 yrs of age who had survived the acute stage of Pneumocystis carinii pneumonitis. Each child was asymptomatic. Spirometric indices, expiratory flows, pulmonary gas transfer factor, arterial blood gases, and other clinical variables were assessed a few days before patients were discharged from the hospital and at 1-, 3-, 6-, and 12-month intervals thereafter; two patients developed recurrent pneumonitis during follow-up and were studied twice. All but five subjects had pulmonary dysfunction when tested initially. A decrease in pulmonary gas transfer factor, observed in 17 studies, was the most common abnormality. Restrictive pulmonary disease was seen in 11 studies; an obstructive component, in one. Arterial hypoxemia at rest, while patients were breathing room air, was noted in nine cases. Roentgenographic evidence of bilateral diffuse lung opacities was seen in 11 patients and was positively correlated with decreases in pulmonary gas transfer factor (p less than 0.001). Arterial hypoxemia was significantly related to intrapulmonary right-to-left shunt (p less than 0.001) but not to decreases in pulmonary gas transfer factor, indicating the importance of ventilation-perfusion abnormalities in these patients. Serial follow-up studies disclosed significant improvement in pulmonary function deficits within 1 month and complete resolution by 6 months in all survivors. Recovery was not related to the amount of duration of O2 therapy, to the need for ventilatory support, or to chest roentgenographic abnormalities. Histopathologic findings in nine patients who died during follow-up did not indicate any residual interstitial fibrosis, collagen deposits, or alveolopathy. We conclude that Pneumocystis carinii pneumonitis during childhood does not typically produce long-lasting pulmonary sequelae.
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PMID:Course of pulmonary dysfunction in children surviving Pneumocystis carinii pneumonitis. A prospective study. 697 3

The value of determination of pleural fluid glucose, pH, lactic dehydrogenase, IgG, IgA, IgM, C3, C4, anti-IgG antibody, and hydroxyproline in distinguishing between pleural effusions caused by rheumatoid arthritis (RA) and those resulting from other diseases was studied. The series comprised seven patients with RA and 115 patients with other diseases including systemic lupus erythematosus, tuberculosis, malignant disease, empyema, pneumonia, congestive heart failure, and nonspecific pleural effusion. The low glucose concentration, the low pH and the low C4 level in rheumatoid pleural effusion were the most valuable diagnostic findings. The presence of anti-IgG antibody in pleural fluid was not specific for RA. The concentration of hydroxyproline in pleural fluid and the pleural fluid-to-plasma hydroxyproline ratio were significantly higher in RA than in tuberculosis and malignant disease. The results support the view that local metabolic and immunological phenomena as well as a high turnover of collagen occur in the pleural cavity in RA.
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PMID:Chemical and immunological features of pleural effusions: comparison between rheumatoid arthritis and other diseases. 698 Dec 26

Highly purified type-specific anti-collagen antibodies (prepared in animals to types I, II, III, and IV bovine collagen) were used in an indirect immunofluorescence method for the study of human lung collagen. The tissue localisation of each collagen type, and the apparent type I:III collagen ratio was assessed in normal foetal and adult lung and in fibrotic lung lesions. In the latter, the relationship of the findings to the natural history of the lesion was considered. This method was compared with routine connective tissue stains. The following observations were made. (1) Foetal lung in the canalicular phase of development proved a useful substrate for validating and standardizing the procedure. (2) Collagen fluorescence was more sensitive than connective tissue stains in detecting collagen in foetal tissues and sites of early fibrosis. (3) On the basis of collagen-type fluorescence, two distinctive patterns of fibrosis were recognised. Areas of mature collagen surrounding vessels and bronchi and in established scar tissue, for example in asbestotic pleural plaques, were virtually exclusively type I collagen. By contrast, areas of early active fibrosis like sarcoid nodules and organising pneumonia, which usually contained variable numbers of fibroblasts and chronic inflammatory cells, were characterised by an increased proportion of type III collagen and a greater intensity of both types I and III collagen fluorescence. The possible significance of this change in type III:I collagen ratio is discussed. Determination of the stage of fibrotic lesions by this method might have applications in the prediction of disease progression, and influence management of some conditions.
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PMID:Immunohistochemical study of collagen types in human foetal lung and fibrotic lung disease. 703 77

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.
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PMID:Structure of alveolar epithelial cells in patients with fibrotic lung disorders. 705 89

Model experiments in white mice reproduced chronic ornithosis pneumonia morphological features of which included early outgrowth of connective tissue cells of the type of carnification, considerable accumulation of tropoglycogen, and disturbed process of collagen fibers formation at a minimal number of leukocytes. Such foci occur in the lungs very early, before the onset of the clinical signs of the disease which appears to be a typical feature of ornithosis pneumonia and may explain causes and mechanisms of frequent occurrence of chronic forms of this disease. In cases of significant multiplication of the ornithosis agent there is mass migration of leukocytes into the focus of lesion followed by the development of acute inflammation. Being an obligatory intracellular parasite, the ornithosis agent affects both large and small alveolar cells. Multiplying by binary division, it stays free in the cytoplasm without forming a common vacuole. Ultrastructurally typical various forms of the ornithosis agent reflecting the stages of its complicated life cycle have been detected.
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PMID:[Pathomorphology of experimental ornithosis pneumonia]. 708 98

An experimental model of nonbacteremic pneumonia with a virulent strain of Pseudomonas aeruginosa was successfully established in guinea pigs immuno-suppressed with cortisone acetate although the organisms were eliminated rapidly from the lungs without cortisone treatment. Using a pocket nebulizer, almost all the animals which received 10(6) organisms/g-lung developed bronchopneumonia without any septic findings as long as 10 days after challenge. The lesions produced in such animals were characterized by dissemination of multiple purulogranulomatous changes. In the early stage of infection, infiltration of polymorphonuclear cells (PMNs) in the bronchiolar and alveolar spaces was diffuse, later showing multifocal accumulation with the formation of central spherical grains enclosing bacterial colonies. In the later stage, granulation tissue consisting of large mononuclear cells, fibroblasts and collagen fibers developed around the PMN accumulation. The animals which received 10(7) organisms/g-lung, on the other hand, developed severe pulmonary hemorrhages and necrosis followed by septic death.
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PMID:Nonbacteremic pseudomonas pneumonia in immunosuppressed guinea pigs. 708 2


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