Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0206061 (interstitial pneumonia)
 6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The synthesis of collagen and EIIIA-containing cellular fibronectin in certain forms of pulmonary fibrosis occurs in discrete locations: in the Masson bodies in bronchiolitis obliterans with organizing pneumonia and in focal clusters of fibroblasts (fibroblastic foci) within airspaces in usual interstitial pneumonia. These sites were examined by electron microscopy and immunohistochemistry using antibodies against cytoskeletal markers and extracellular matrix components in biopsies from three patients with bronchiolitis obliterans with organizing pneumonia and four patients with usual interstitial pneumonia. Fibroblasts of both Masson bodies and fibroblastic foci expressed vimentin and alpha smooth muscle actin but not desmin, distinguishing them from true smooth muscle. In both structures fibroblasts with well-formed actin filament bundles were aligned parallel to one another, enmeshed in a matrix of fibronectin-containing fibrils (microtendons) that linked cells and collagen bundles. Similar features characterize the phase of contraction during the healing of skin wounds. This suggests that active contractions of fibroblasts plays a role in the remodeling of the lung in pulmonary fibrosis.
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PMID:The roles of the myofibroblast in idiopathic pulmonary fibrosis. Ultrastructural and immunohistochemical features of sites of active extracellular matrix synthesis. 202 10

Immunohistochemical methods were used to distinguish idiopathic pulmonary fibrosis (IPF) from interstitial pneumonia associated with rheumatoid arthritis (RA lung). The subjects were six patients with IPF and seven with RA lung, in whom the pathological findings were consistent with usual interstitial pneumonia. Antibodies to vimentin (Vim), alpha-smooth muscle actin (alpha-SMA), and S-100 protein were used for immunohistochemical studies done by the streptavidin-biotin-peroxidase complex method. In fibrosis associated with RA lung, proliferation of both Vim and alpha-SMA-positive myofibroblasts was widely observed, despite pathological findings of honeycombing, usual interstitial pneumonia, and BOOP. Fibrosis in cases of IPF was found to be characterized mainly by Vim-positive fibroblasts, and on occasion was associated with hyperplasia of smooth muscle. Lung tissues from patients with acute exacerbations of RA lung, especially when associated with a BOOP pattern, had many cells positive for S-100 protein. However, such cells were generally hard to find in cases of IPE. Similar results were obtained with regard to the honeycomb pattern in both IPF and RA lung. These findings suggest that IPF and RA lung can be fairly clearly differentiated based on the proliferation of myofibroblasts and on the presence or absence of cells positive for S-100 protein.
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PMID:[Immunohistochemical study of fibrosis and S-100 protein-positive cells in idiopathic pulmonary fibrosis and in interstitial pneumonia associated with rheumatoid arthritis]. 871 85

We present a comparative histopathological study of both acute and chronic human adenovirus pneumonia, with reference to the cellular and extracellular matrix components. Seventeen lungs from autopsied patients whose ages ranged from 2 to 60 months were studied. Adenovirus types 1, 2, 3, 5, and 7 were isolated from 15 patients with acute lung disease, and types 2 and 7 were isolated from the other two patients with chronic pulmonary illness. The results indicated the occurrence of two basic patterns of adenovirus interstitial pneumonia (1) classic pattern (acute), characterized by necrosis and degeneration and many type II pneumocytes with intranuclear inclusion bodies, which were positive for adenovirus DNA by in situ hybridization, and (2) proliferative or proliferative-productive pattern (chronic), which presented with diffuse pulmonary fibrosis and the interstitial proliferation of fibroblast-like cells, compatible with myofibroblasts (positive for vimentin and alpha smooth muscle actin), and increase in collagen types I and III, elastic fibers, and proteoglycans. Alveolar collapse appears to be an important pathogenetic mechanism in the development of this pattern.
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PMID:Acute and chronic human adenovirus pneumonia: cellular and extracellular matrix components. 902 50

Immunohistochemical study was carried out in patients with collagen vascular disease associated with interstitial pneumonia. The subjects were 16 patients, consisting of seven rheumatoid arthritis (RA), five dermatomyositis (DM) and four progressive systemic sclerosis (PSS), in whom the pathological findings were consistent with usual interstitial pneumonia. Immunohistochemical examinations were performed by the ABC method using antibodies to vimentin (vim), alpha-smooth muscle actin (alpha-SMA), and S-100 protein. In fibrosis associated with RA, proliferation of alpha-SMA-positive myofibroblasts was widely observed in all subjects. Myofibroblasts were present also in patients with DM and PSS, but not as notable as in those with RA. Proliferation of vim-positive fibroblasts was observed in patients with idiopathic pulmonary fibrosis (IPF). Diverse S-100 protein positive cells appeared in patients with acute exacerbations of RA, especially when associated with bronchiolitis obliterans organizing pneumonia (BOOP) pattern. S-100 protein positive cells were observed occasionally also in patients with DM and PSS, but they markedly decreased in number, compared to those with RA. They were generally hard to detect in lungs of patients with IPF. These findings suggest that interstitial pneumonia associated with collagen vascular disease can be fairly clearly differentiated from IPF each other, based on the degree of proliferation of myofibroblasts and on the presence of S-100 protein positive cells in number.
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PMID:[Immunohistochemical study of myofibroblast and S-100 protein positive cells in interstitial pneumonia associated with collagen vascular disease]. 912 18

Pulmonary fibrosis resulting from increased accumulation of various extracellular matrices is a prominent feature in chronic progressive lung diseases. Heat shock protein 47 (HSP47) is a collagen-binding stress protein known to have a specific role in the intracellular processing of procollagen molecules as a collagen-specific molecular chaperone in various organs. Possible involvement, however, of HSP47 in relation to increased deposition of collagens in fibrotic lung diseases is not yet known. In this study, we investigated the expression of HSP47 in various pulmonary fibrotic diseases. Formalin-fixed, paraffin-embedded lung sections from 17 autopsies of patients with various pulmonary fibrotic diseases, e.g., organizing pneumonia, interstitial pneumonia, idiopathic pulmonary fibrosis, and diffuse alveolar damage, were stained with monoclonal antibodies for alpha-smooth muscle actin, vimentin, CD68, Type III collagen, and HSP47. The extent of staining was graded semiquantitatively. Five control lung sections were also simultaneously studied. The fibrotic lung sections, in comparison with the control sections, had more interstitial cells positive for alpha-smooth muscle actin and fibroblasts positive for vimentin; we also saw increased infiltration of CD68-positive macrophages. For HSP47, in comparison with the control lung sections, markedly increased immunostaining was always noted in the fibrotic lung sections in association with increased accumulation of Type III collagen in the fibrotic masses. By double immunostaining, colocalization of collagens and HSP47 was noted in the regions of pulmonary fibrosis, and HSP47-expressing cells were found to be mainly alpha-smooth muscle actin-positive interstitial cells. From the above observations, we concluded that overexpression of HSP47 might play an important role in the excessive assembly/synthesis of collagens and could thereby contribute to the fibrosis found in pulmonary fibrotic lung diseases.
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PMID:Immunolocalization of collagen and collagen-binding heat shock protein 47 in fibrotic lung diseases. 987 49

The aim of this study was to investigate whether idiopathic pulmonary fibrosis (IPF) can be distinguished from rheumatoid arthritis (RA)-associated interstitial pneumonia (RA-IP) by means of quantitatively assessing myofibroblasts and S-100 protein positive dendritic cells. Seven patients with IPF and twelve with RA, in whom the pathological findings were consistent with usual interstitial pneumonia (UIP) were studied. Antibodies to vimentin, alpha-smooth muscle actin (alpha-SMA) and S-100 protein were used for immunohistochemical studies performed using the streptavidin/biotin/peroxidase complex method, applied to dewaxed sections from each case. In fibrosis of RA-IP, appearance of both vimentin- and alpha-SMA-positive cells, namely myofibroblasts, was widely observed, together with the pathological patterns of honeycombing, UIP and bronchiolitis obliterans-organizing pneumonia (BOOP). Fibrosis, in cases of chronic IPF, was found to be characterized mainly by vimentin-positive but alpha-SMA-negative fibroblasts. Pulmonary tissues from RA-IP patients especially when associated with a BOOP pattern, contained many cells positive for S-100 protein. However, such cells were generally hard to find in cases of IPF. These findings suggests that idiopathic pulmonary fibrosis and rheumatoid arthritis-associated interstitial pneumonia can be differentiated from each other, to some extent, based on the appearance of myofibroblasts and the presence of S-100-positive dendritic cells.
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PMID:Myofibroblasts and S-100 protein positive cells in idiopathic pulmonary fibrosis and rheumatoid arthritis-associated interstitial pneumonia. 1054 78

It has been suggested that the humoral immune system plays a role in the pathogenesis of non-specific interstitial pneumonia (NSIP). Although some circulating autoantibodies to cytoskeletal protein(s) have been suggested, the antimyofibroblast antibody has not been investigated in patients with idiopathic pulmonary fibrosis (IPF) and NSIP. The purpose of this study is to evaluate the existence of antimyofibroblast antibody in the sera of patients with IPF and NSIP. The MRC5 cell line was used as a model of myofibroblast. The anti-MRC5 cell antibody was characterized in a patient with NSIP using Western blotting. Since we found that one of the anti-MRC5 antibodies was an antivimentin antibody, we established an enzyme-linked immunosorbent assay (ELISA) to measure the levels of antivimentin antibody in the sera of patients with IPF (n = 12) and NSIP (n = 23). Initially, two anti-MRC5 cell antibodies were detected in the sera of patients with NSIP, one of which was characterized as the antivimentin antibody by Western blotting. The other was characterized as an antivimentin fragment antibody. We established an ELISA to measure the antivimentin antibody and found significantly higher levels in patients with IPF and NSIP than in normal volunteers. One of the anti-MRC5 cell antibodies in the serum of a patient with NSIP was against vimentin. The serum levels of antivimentin antibody were increased in patients with IPF and NSIP compared with that of normal volunteers. These results suggest that the antivimentin antibody may be involved in the process of lung injury in IPF and NSIP.
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PMID:Detection of antivimentin antibody in sera of patients with idiopathic pulmonary fibrosis and non-specific interstitial pneumonia. 1198 5

We report a rare case of a primary intracerebral malignant fibrous histiocytoma (MFH) with malignant progression from a premalignant stage. A 73-year-old male presented with mild hemiparesis on the right side of his body 4 months prior to admission. MR images showed a homogenously enhanced mass in the left parietal lobe. The patient underwent an uneventful extirpation of the solid mass. Microscopically, the solid tumor contained histiocytic cells and spindle-shaped fibroblastic cells arranged in a storiform pattern. The tumor cells were immunoreactive for vimentin, MAC 387 (macrophage marker) and alpha-1-antitrypsin. The MIB-1-positive rate was 1%. The histological diagnosis was fibrous histiocytoma. Postoperative MR images demonstrated no abnormally enhanced lesions. The patient's neurological symptoms and signs gradually improved. One year after surgery, he developed right hemiparesis. MR images showed a heterogeneously enhanced mass in the left sensorimotor area. This recurrent tumor was totally resected. Microscopically, the tumor was composed of atypical spindle-shaped cells, forming a storiform pattern. Pleomorphism was prominent, and necrotic foci were also seen. The MIB-1 labeling index averaged 11%. The histological findings corresponded to those of MFH. Unfortunately, the patient died of interstitial pneumonia contracted during postoperative radiotherapy. Early detection and resection at a stage of low malignant potential, followed by radiochemotherapy, are crucial for the management of this mesenchymal tumor.
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PMID:[Primary intracerebral malignant fibrous histiocytoma: case report]. 1249 83

In a previous study, we demonstrated anti-vimentin antibodies in sera of patients with interstitial pneumonia. We hypothesized that antibodies in sera might detect vimentin fragments formed during the process of apoptosis. To prove this, recombinant human vimentin was digested by recombinant human caspase-3 or caspase-8. Then, Western blotting using several commercially available antibodies against human vimentin or patients' sera which had anti-vimentin autoantibodies, was performed. As a result, after recombinant human vimentin was digested by caspase-3 or caspase-8, several vimentin fragments were formed and detected by 2 kinds of monoclonal anti-vimentin antibodies (clone 3B4 and clone V9) as well as by polyclonal sheep anti-human vimentin antibody. It was demonstrated that high molecular weight vimentin was formed after the digestion of vimentin by caspase-3, which was only detected by patients' sera. The high molecular weight vimentin was not formed after digestion of vimentin by caspase-8. Our present results show that high molecular weight vimentin was formed after the digestion of vimentin by caspase-3. In addition, it is suggested that this high molecular weight vimentin acted as an autoantigen to form anti-vimentin autoantibody in vivo.
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PMID:High molecular weight vimentin complex is formed after proteolytic digestion of vimentin by caspase-3: detection by sera of patients with interstitial pneumonia. 1290 5

Minute pulmonary meningothelial nodules are rare lesions histologically composed of small nests of epithelioid cells located within the interstitium of the lung. These nodules are generally asymptomatic and are usually found incidentally at autopsy or in surgical specimens resected for unrelated causes. The lesions are most often single, although multiple lesions with unilateral involvement of one or even all lobes of the same lung have been described. To our knowledge, cases of meningothelial nodules with disseminated bilateral pulmonary involvement associated with clinical symptoms of restrictive pulmonary disease and radiologic evidence of diffuse reticulonodular pulmonary infiltrates have not been previously documented. We have studied 5 patients presenting with diffuse bilateral pulmonary involvement by numerous minute pulmonary meningothelial nodules. The patients were 4 women and a man aged 54 to 75 years who presented clinically with dyspnea and shortness of breath and the lesions were discovered on open lung biopsies performed for the evaluation of diffuse bilateral interstitial lung infiltrates found on chest x-rays and computed tomography scans. In 3 patients, there was a previous history of malignancy and the radiologic findings were suspected of representing diffuse metastatic disease. Histologically, the lesions were composed of small clusters of epithelioid cells with round to oval nuclei devoid of atypia and surrounded by abundant eosinophilic cytoplasm. Immunohistochemical studies showed positivity of the tumor cells for epithelial membrane antigen and vimentin, and negative staining for cytokeratin, actin, S-100 protein, CD34, chromogranin, and synaptophysin. Electron microscopic examination in 1 case confirmed the ultrastructural features of meningothelial cells, including complex cytoplasmic interdigitations joined by well-developed desmosomes and abundant intracytoplasmic intermediate filaments. The diffuse bilateral involvement of lung parenchyma in the present cases can lead to confusion on clinical and radiologic grounds with a variety of interstitial pulmonary processes, including idiopathic interstitial pneumonia and lymphangitis carcinomatosa. Diffuse pulmonary meningotheliomatosis should be considered in the clinical differential diagnosis of diffuse interstitial pulmonary infiltrates.
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PMID:Diffuse pulmonary meningotheliomatosis. 1741 11


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