Showing papers by "Talmadge E. King published in 1989"
TL;DR: Fibrosis in chronic idiopathic pulmonary fibrosis results mainly from organization of exudate within airspaces, just as it does after acute lung injury, and during this process, fibroblasts increase their synthesis of collagen and fibronectin coordinately.
Abstract: Fibroblasts in healthy adult lung are quiescent, synthesizing little collagen. We studied lung biopsies from 30 patients with pulmonary fibrosis, using immunohistochemistry with monoclonal antibodies against the propeptides of type I collagen to localize fibroblasts actively synthesizing collagen. Adjacent sections were stained with antibodies to type III and IV collagen, fibrin, cytokeratin, plasma fibronectin, or EDIIIa-containing "cellular" fibronectin (cFN). In rapid pulmonary fibrosis, including the proliferative phase of diffuse alveolar damage, organizing pneumonia, and subacute idiopathic fibrosis, collagen-synthesizing cells were numerous in organizing exudate filling airspaces but were also seen in the interstitium of the alveolar walls, interlobular septa, and walls of blood vessels. The new matrix deposited in the airspaces also contained type III collagen and EDIIIa-containing fibronectin. In chronic pulmonary fibrosis, more than half of the biopsies showed foci of collagen synthesis and cFN deposition near the air-tissue interface. The foci were consistently localized outside remnants of basal lamina and therefore within airspaces. The results indicate that (1) fibrosis in chronic idiopathic pulmonary fibrosis results mainly from organization of exudate within airspaces, just as it does after acute lung injury, and (2) during this process, fibroblasts increase their synthesis of collagen and fibronectin coordinately. Foci of active matrix deposition provide evidence for the progressive nature of chronic pulmonary fibrosis.
446 citations
TL;DR: The case presented here was acute in onset, suggesting a hypersensitivity reaction, and the patient rapidly improved with corticosteroid therapy, and there was no evidence of an infectious etiology.
Abstract: A previously healthy young man presented with acute respiratory distress and diffuse bilateral infiltrates on chest radiograph. Eosinophilic pneumonia was diagnosed by bronchoalveolar lavage and confirmed by transbronchial lung biopsy. There was no evidence of an infectious etiology, and the patient rapidly improved with corticosteroid therapy. Most cases of eosinophilic pneumonia reported previously have followed a chronic course. The case presented here was acute in onset, suggesting a hypersensitivity reaction. High levels of bronchoalveolar lavage eosinophils indicate the diagnosis but not the etiology of eosinophilic pneumonia.
179 citations
TL;DR: It is concluded that use of fiberoptic bronchoscopy with transbronchial biopsy and BAL facilitates diagnosis of beryllium workers who have histopathologic and immunologic alterations consistent with chronic beryLLium disease.
Abstract: Beryllium lung disease is a chronic granulomatous disorder in which a beryllium-specific immune response plays a central role. By using a measure of cellular immune response to beryllium salts, bronchoalveolar lavage (BAL), and lung biopsy, we have identified 12 new cases of beryllium disease. Each of these individuals had pathologic changes on biopsy, lymphocytic alveolitis on BAL, and positive BAL lymphocyte transformation tests (LTT) in response to beryllium sulfate. This group of patients was remarkable for its paucity of clinical findings. At initial evaluation, seven had no respiratory symptoms, and four had normal physical examinations. Five had no increase in interstitial markings on chest radiograph. In eight cases, flow rates and lung volumes were normal. Diffusing capacity for carbon monoxide was low in only one case, and oxygen exchange during exercise was normal in six of nine subjects studied. In addition to the 12 cases, we evaluated eight beryllium-exposed workers who had other (nonberyllium) lung diseases; two of these eight demonstrated beryllium sensitization based on BAL LTT. We conclude that use of fiberoptic bronchoscopy with transbronchial biopsy and BAL facilitates diagnosis of beryllium workers who have histopathologic and immunologic alterations consistent with chronic beryllium disease. These findings may precede frank clinical illness and physiologic impairment, having important implications for our understanding of the natural history of beryllium disease.
169 citations
TL;DR: Alveolar macrophages from patients with IPF express a functional deficiency in their ability to kill facultative intracellular bacteria, and it does not appear that this defect in bactericidal activity in IPF macrophage results from a defect in the antigen-presenting function of these cells.
Abstract: The accumulation of inflammatory and immune effector cells in the lungs of patients at early stages of Interstitial lung disease has been well documented, but little is known about the functional activity of these cells, particularly alveolar macrophages. The purpose of the experiments described here was to determine whether alveolar macrophages from patients with idiopathic pulmonary fibrosis (IPF) differed from alveolar macrophages of normal subjects using a model system that assesses a component of cell-mediated immunity. Alveolar macrophages were tested for their ability to phagocytose and kill the facultative intracellular bacterium Listeria monocytogenes. Because this system requires the stimulation of macrophages by antigen-specific T-cells, it allows the assessment of effector functions of macrophages found in the lower respiratory tract of patients with IPF. Data showed that alveolar macrophages from normal subjects both phagocytosed and killed those bacteria. However, alveolar macrophages from p...
13 citations