Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phenotype of alveolar macrophages (AMs) is known to be modulated during pathological immune reactions in the lung. In this study, we wanted to determine the relationship between the AM phenotype and changes in the proportions of the various immune cells in bronchoalveolar lavage (BAL). BAL was performed in 76 consecutive patients, including 32 with sarcoidosis, 8 with idiopathic pulmonary fibrosis, 9 with pneumoconiosis, 13 with other respiratory disorders, and 14 controls without evidence of interstitial lung disease. The phenotype of AMs was studied by a panel of 15 monoclonal antibodies against various myeloid antigens, and was correlated with the proportions of cells obtained by BAL. The percentage of BAL lymphocytes showed a relationship with the expression of macrophage antigens in 11 out of 15 antigens studied (all except adhesive molecules CD11a, CD11c, CD18 and the antigen 25F9 present on mature macrophages). Furthermore, the CD4/CD8 ratio of BAL T-lymphocytes correlated with the AM expression of CD54 (intercellular adhesion molecule-1 (ICAM-1)), RFD1 (marker of dendritic cells), and CD71 (transferrin receptor). In samples with an increased number of bronchoalveolar neutrophils, the subpopulation of 27E10 positive AMs (inflammatory acute phase macrophages) was increased. Eosinophils in BAL were not associated with a significant increase in AM membrane antigen expression. Prominent changes of the AM phenotype were found in active sarcoidosis showing lymphocytic alveolitis, with more frequent expression of CD54, KiM2, CD71, CD11b and RFD9. In conclusion, this study shows that the phenotype of AMs is related to the type and intensity of the immunopathological reaction in the lung, and correlates with the proportions of bronchoalveolar cells.
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PMID:The phenotype of alveolar macrophages and its correlation with immune cells in bronchoalveolar lavage. 790 72

To identify the clinical relevance of cytokines involved in the development of lung fibrosis observed in patients with coal workers' pneumoconiosis (CWP), we investigated the BAL fluid contents and AM secretions of three mediators that modulate fibroblast growth: platelet-derived growth factor (PDGF), Type I insulin-like growth factor (IGF-I), and transforming growth factor Type beta (TGF-beta). Our study population consisted of 25 patients with CWP (16 simple pneumoconiosis, SP, 9 progressive massive fibrosis, PMF, 9 control subjects, and 6 patients with idiopathic pulmonary fibrosis (IPF). The fibrotic potency of AM supernatants was also tested for their ability to promote the growth of a human lung fibroblast cell line appreciated by [3H]-thymidine incorporation. PDGF and IGF-I concentrations were increased in BAL fluids of patients with PMF compared with SP and control subjects, whereas TGF-beta concentration was significantly higher in BAL fluid of patients with SP compared with PMF and control subjects. PDGF, IGF-I, and TGF-beta concentrations in AM supernatants followed the same profile observed in BAL fluids, suggesting that AM is one of the main cell sources of PDGF, IGF-I, and TGF-beta in the lung of pneumoconiotic patients. After treatment by acidification, which activated the latent form of TGF-beta, AM from patients with SP induced an inhibition of [3H]-thymidine incorporation and fibroblast growth was restored after neutralization of TGF-beta by specific antibodies. In contrast, AM supernatants from patients with PMF and IPF promoted the proliferation of fibroblasts and treatment by acidification did not modify this effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of fibrosis in coal workers' pneumoconiosis. Increased production of platelet-derived growth factor, insulin-like growth factor type I, and transforming growth factor beta and relationship to disease severity. 792 35

Since 1983 unilateral lung transplantation has become a clinical reality. The initial experience of the Hospital General Universitario de la Vall d'Hebron is presented with the description of the two first unipulmonary transplants. The first was a 20 year-old woman with idiopathic pulmonary fibrosis in whom a left unipulmonary transplant was carried out and who, at present is at home following the 23rd postoperative month. The second case was a 27 year-old man with pneumoconiosis who, at 12 months following the left lung transplantation, carries on a normal life. Among the complications observed, the presence of pneumonitis by cytomegalovirus in both patients is of note. Stenosis and partial dehiscence of the bronchial suture in the first patient and isolation of syncitial respiratory virus in the second patient were also observed. The effort and integration into a normal life style of the second patient is excellent. In contrast, the first patient presents an important postoperative functional deterioration secondary to her complications. The present study demonstrates that unipulmonary transplantations is a reality in Spain which must be considered by all respiratory disease specialists in their daily clinical practise.
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PMID:[Unilateral lung transplantation: the first 2 cases. Group of Lung Transplantation of the University General Hospital of the Vall d'Hebron]. 847 82

Fibrosis is a disorder characterized by a qualitative and quantitative alteration of the deposition of extracellular matrix with accumulation of mesenchymal cells in replacement of normal tissue. The sequence of events leading to fibrosis of an organ involves the subsequent processes of injury with inflammation and disruption of the normal tissue architecture, followed by tissue repair with accumulation of mesenchymal cells in this area. A similar sequence of events occurs in wound healing with formation of normal, limited and transient granulation tissue, while in fibrosis, a maladaptive repair leads to an extensive, exaggerated process with functional impairment. Inflammatory cells (mainly mononuclear phagocytes), platelets, endothelial cells, and type II pneumocytes play a direct and indirect role in tissue injury and repair. The evaluation of several human fibrotic lung diseases, five diffuse (idiopathic pulmonary fibrosis (IPF); adult respiratory distress syndrome (ARDS); coal workers' pneumoconiosis (CWP); Hermansky-Pudlak syndrome (HPS); systemic sclerosis (SS)) and two focal (tumour stroma in lung cancer; and obliterative bronchiolitis (OB) after lung transplantation), has shown that several cytokines participate in the local injury and inflammatory reaction (interleukin-1 (IL-1), interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), and tumour necrosis factor-alpha (TNF-alpha)), while other cytokines are involved in tissue repair and fibrosis (platelet-derived growth factor (PDGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-beta), and basic-fibroblast growth factor (b-FGF)). A better understanding of the cytokines and cytokine networks involved in lung fibrosis leads to the possibility of new therapeutic approaches.
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PMID:The role of cytokines in human lung fibrosis. 868 Mar 82

It is well known that silica exposure leads in an experimental model to the development of an acute fibrotic process. In human beings two main observations have already been done: (1) silica exposure is frequently associated with the development of connective tissue disease (CTD), especially progressive systemic sclerosis; (2) 10 to 20% patients with CTD developed pulmonary fibrosis. In this context we report 26 cases of coal miners who presented with clinical, radiological, biological and functional characteristics mimicking idiopathic pulmonary fibrosis (IPF), with or without associated coal worker's pneumoconiosis (CWP). All were men; mean age was 68 +/- 9.2 years. Twenty-three were smokers. Duration of exposure was 28.8 +/- 9.1 years. All the patients had dyspnea (stage III, IV in the NHYA classification) and diffuse crackles. Eleven out of 26 had finger clubbing. Computed tomography showed honeycombing (23 cases), and/or ground glass opacities (6 cases) with bronchiectasis (3 cases) predominant in the lower lobes; 19 had radiological signs of CWP, micronodules (n = 16) and nodules (n = 3) predominant in the upper lobes. BAL exhibited an increased % of neutrophils (11.9 +/- 16.1%). Lung function demonstrated a restrictive pattern (TLC = 73 +/- 15.6% and VC = 80 +/- 18% of predicted values) associated with a decreased DLCO (51.8 +/- 23.6% of predicted values) and hypoxemia (at rest = 66.5 +/- 11.2 mmHg, upon effort = 56 +/- 12 mmHg). Lung biopsies were performed in four cases and demonstrated interstitial fibrosis of intraalveolar septum with an accumulation of immune and inflammatory cells similar to the one described in IPF. The association between IPF and silica exposure with or without associated CWP points out the problem of legal recognition of idiopathic-like pulmonary fibrosis as a complication of the occupational exposure of coal workers.
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PMID:["Primary" diffuse interstitial fibrosis in coal miners: a new entity? Study Group on Interstitial Pathology of the Society of Thoracic Pathology of the North]. 941 11

Elevated levels of serum surfactant protein-D (SP-D) have been previously reported in patients with idiopathic pulmonary fibrosis (IPF) and pulmonary alveolar proteinosis. To determine whether the same change is seen in other pulmonary diseases, especially pulmonary tuberculosis (TB), we measured the serum SP-D levels in active pulmonary TB (smear and/or culture: positive), acute interstitial pneumonia (AIP), IPF, acute exacerbation of IPF, hypersensitivity pneumonitis (HP), pneumoconiosis, bronchiectasis, and bacterial pneumonia by an enzyme-linked immunosorbent assay using monoclonal antibodies to human lung SP-D, and compared them with those of healthy elderly subjects over 50 years of age. The SP-D level in the healthy elderly subjects was 57.6 +/- 38.4 ng/ml (mean +/- SD, n = 287). The levels in patients with active pulmonary TB (140.6 +/- 18.2 ng/ml, n = 49), AIP (1,021 ng/ml, n = 1), IPF (307.0 +/- 180.7 ng/ml, n = 42), acute exacerbation of IPF (817.7 +/- 283.6 ng/ml, n = 3), and HP (716.6 +/- 548.8 ng/ml, n = 4) were significantly higher than those in the healthy elderly controls (p < 0.05), whereas those of pneumoconiosis, bronchiectasis, and bacterial pneumonia, 121.9 +/- 92.8 ng/ml (n = 8), 93.9 +/- 72.9 ng/ml (n = 11), and 72.7 +/- 3.4 ng/ml (n = 4), respectively, showed no significant difference with the controls. In active pulmonary TB, the percentage of patients whose serum SP-D levels were over 134.6 ng/ml (mean + 2SD of healthy elderly controls) was 34.7%, and therefore we considered the serum SP-D level was not useful for the diagnosis of pulmonary TB. However, it was significantly higher in the patients with cavity formation than in those without (p < 0.05), and there was a significant positive correlation between the serum SP-D level and the number of tubercle bacilli in the sputum (r = 0.416, p = 0.00165), erythrocyte sedimentation rate at 1 hr (r = 0.489, p < 0.01), and CRP level (r = 0.383, p = 0.003). These findings suggest that the serum SP-D level is a useful indicator of the disease activity in pulmonary TB.
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PMID:[Significance of serum surfactant protein-D (SP-D) level in patients with pulmonary tuberculosis]. 984 46

Pneumoconioses are still a common cause of chronic lung disease. In industrialized countries, improvements in working conditions and dust control measures have led to a decrease in the incidence of severe forms of silicosis, coal worker pneumoconiosis, and parenchymal asbestosis. However, the diversity of settings in which silica and asbestos are used fuels a continued input of cases, and the burden of cases related to remote exposures is still considerable. Overall, the clinical picture of the classic pneumoconioses and their complications has not changed substantially. However, their limits and links have expanded toward systemic and connective tissue disease, idiopathic pulmonary fibrosis, and antineutrophil cytoplasmic autoantibody-positive vasculitides. Immunologically mediated occupational lung diseases have emerged, such as berylliosis and hard-metal disease. Advances in imaging, mineralogic analysis of bronchoalveolar lavage fluid, and immunologic techniques have been instrumental in describing new patterns of disease and are helpful in litigious or difficult cases.
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PMID:The past and present of pneumoconioses. 1074 76

We investigated the indications for lung transplantation (LTx) in Japan and discussed questions regarding the current Japanese criteria of LTx. This study examined 37 patients referred to our institute for LTx. Among these patients, there were 11 cases of primary pulmonary hypertension (PPH), 6 of lymphoangiomyomatosis (LAM), 4 of Eisenmenger's syndrome, 3 of bronchiolitis obliterans, 2 each of bronchiectasis, idiopathic pulmonary fibrosis (IPF), and pneumoconiosis, and 7 of other diseases. The most frequent age group was 30-39 years (12 cases, 32.4%), and more than half of the patients were female (22 cases, 59.5%). The regions of residence of the patients were Tohoku (19 patients), Kanto (16), and Chubu (2). Patients were referred from all over eastern Japan. On evaluation, LTx was contraindicated in 5 cases, in 4 of which mechanical ventilation had been installed before consultation with us. Six patients died before registration on the Japan Organ Transplant Network (JOT). 6 transplant candidates were registered with JOT, but one (PPH) died after 6 months of waiting, and one (LAM) received a lung transplant from a brain dead cadaver donor. We propose to reform and clarify the Japanese criteria for LTx-both indications and contraindications, to include such indications as a survival probability of less than two years, and such contraindications as mechanical ventilation. Early consultation at LTx centers was hoped for, in accordance with the International Guidelines and a transplant window.
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PMID:[Clinical analysis of patients referred for lung transplantation in eastern Japan]. 1119 18

Chronic interstitial lung diseases including pneumoconiosis have pathological characteristics which alter the lung structure and function consequent to the accumulation and activation of inflammatory cells in the lower respiratory tract. These activated cells usually secrete the inflammatory and fibrogenic mediators. Of the diffuse parenchymal lung diseases, the majority have no known etiology and idiopathic pulmonary fibrosis (IPF) is the diagnosis most frequently encountered by clinicians. Pathogenic similarities between pneumoconiosis and IPF provide a strong basis for hypothesizing that environmental agents may cause IPF. Many case-control studies have been published that provide further evidence for a number of associations between occupational and environmental exposures and IPF. Such reports support a strong evidence that IPF may be a heterogenous disorder associated with a number of environmental exposures. As a model of lung fibrosis, experimental pneumoconiosis is giving us a great information because crystalline silica is probably one of the most typical agent producing pulmonary fibrosis and the severity of its health effects and the widespread nature of exposure have been long recognized. Many papers provide evidence that particles have the potential to cause stimulation of phagocytes to release oxidants and such oxidative stress is believed to be a major factor in pulmonary inflammation followed by fibrotic change. Many kinds of cellular mediators are recognized as a implicating factor in this process including cell-to-cell interaction, enzymes, cytokines, arachidonic acid derivatives et al. Treatment of pneumoconiosis is an attractive and interesting topic. But, the mechanism of pathogenesis of pneumoconiosis is not thoroughly understood yet. Also, whether the process of fibrosis formation be retarded or not is questionable with some therapeutic trial. Therefore, a sensitive biomarker which is possible to estimate the pathological pathway in pneumoconiosis is needed. Our laboratory has studied particulate-induced pulmonary reaction for two decades consistently. This review will focus on signal transduction pathway involved in oxidative stress and some inhibitory agents with pleiotropic mechanism in pulmonary fibrosis. I will also introduce some data of animal studies with multidrug regimen as well.
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PMID:Recent advances in particulate-induced pulmonary fibrosis; for the application of possible strategy experimentally and clinically. 1146 77

Clinical-and-biological, biochemical, immunological, histomorphological; X-ray and functional examinations of workers of an electric-melting shop manufacturing brass alloys, who had contacts with condensation aerosol with a high zinc oxide concentrations, were used to detect in them pneumoconiosis with the exogenous fibrosing alveolitis (ZEFA). Some workers had acute conditions, i.e. "foundry fever" speaking in clinical terms, which was followed by a period of "visible improvement" lasting on the average for 8.6 +/- 0.8 years. The latter was described by the autoimmune activation of B-lymphocytes accompanied by an intensified formation of circulating immune complexes with a sharp reduction of the DR-cell content. The disease onset is gradual with the below signs: increasing dyspnea, cough and cyanosis of the lips due to the developing hypoxemia with decreasing PO2 (below 80 mm Hg); it can also be displayed through a mixed type of respiratory insufficiency with a lower PO2 and a higher PCO2 (above 40 mm Hg)-X-ray showed reticular changes in the pulmonary pattern. Generation of a high-above-norm quantity of active forms of oxygen and nitrogen by alveolar macrophages and neutrophils in their contacts with cellular membranes is the key mechanism triggering the pathological process like it happens in all cases of pneumoconiosis. Transformation of the mentioned products of free-radical oxygenation into hydroxyl radicals in the catalytic centers of the dust-particle borders containing zinc (which is, like iron, a metal with transient valence) is ZEFA specificity. The factor draws together ZEFA with pathological processes caused by asbestos-fiber dust, which have iron ions in their catalytic centers.
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PMID:[Exogenous fibrosing alveolitis due to the condensation aerosol (smoke) of zinc oxide]. 1510 72


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