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Results for “PULMONARY FIBROSIS”

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At least 811 records · Page 45Linked to original sources
PubMed1988

[Apical pulmonary fibrosis and rheumatoid polyarthritis].

The authors report a case of apical pulmonary fibrosis associated with rheumatoid arthritis. The pulmonary lesions were clearly different from the classical features of pleuro-pulmonary disease in rheumatoid arthritis. They were identical to those described in ankylosing spondylitis. A review of the literature reveals recent report on ten similar cases. The authors discuss a possible relationship with bronchiolitis obliterans.

Arthritis, Rheumatoid↗
PubMed2007

The role of anti-endothelial cell antibody-mediated microvascular injury in the evolution of pulmonary fibrosis in the setting of collagen vascular disease.

We encountered 16 patients with connective tissue disease in whom pulmonary fibrosis developed. Routine light microscopic, ultrastructural, and direct immunofluorescent analyses were conducted, and circulating antibodies, including those of endothelial cell derivation, were assessed using indirect immuno-fluorescence and Western blot assays. Underlying diseases were dermatomyositis, scleroderma, mixed connective tissue disease, sclerodermatomyositis, Sjögren syndrome, rheumatoid arthritis, and anti-Ro-associated systemic lupus erythematosus. Antibodies to one or more Ro, RNP, Jo 1, OJ, and/or nucleolar antigens were seen in all cases and antiphospholipid antibodies in half. All biopsies revealed microvascular injury in concert with intraparenchymal fibrosis; in some cases, there were corroborative ultrastructural findings of microvascular injury. Patterns of fibroplasia represented nonspecific interstitial pneumonitis and usual interstitial pneumonitis. We noted IgG, IgA, and/or complement in the septal microvasculature. In 6 cases with available serum samples, indirect immunofluorescent endothelial cell antibody studies were positive and Western Blot studies showed reactivity of serum samples to numerous endothelial cell lysate-derived proteins. Pulmonary fibrosis, a recognized complication of systemic connective tissue disease, develops in connective tissue disease syndromes with pathogenetically established immune-based microvascular injury at other sites. A similar mechanism of antibody-mediated endothelial cell injury may be the basis of the tissue injury and fibrosing reparative response.

Animals↗
PubMedDate not supplied

[Pulmonary fibrosis secondary to nitrofurantoin].

We report a case of pulmonary fibrosis from long-term furantoin therapy after radical surgery for a bladder tumor and urinary intestinal diversion. The patient developed pulmonary superinfection and acute respiratory failure. She initially responded to treatment, but relapsed two weeks later. The underlying pathological condition led to the patient's death.

Colon, Sigmoid↗
PubMedDate not supplied

Increased extracellular matrix metalloproteinase inducer (EMMPRIN) expression in pulmonary fibrosis.

Extracellular matrix metalloproteinase inducer (EMMPRIN) was examined on bronchoalveolar lavage fluids (BALFs) and lung tissue from patients with fibrosis (usual interstitial pneumonia-idiopathic pulmonary fibrosis [UIP-IPF], n = 15; diffuse parenchymal lung diseases without IPF characteristics on computerized tomography scan, n = 8) and without fibrosis (n = 6). In UIP-IPF, EMMPRIN staining was increased in areas of fibrosis, mainly in macrophages and in epithelial cells. EMMPRIN was also found in the extracellular medium with significant levels in patients with lung fibrosis compared to subjects without fibrosis. Moreover, macrophages from patients with lung fibrosis spontaneously produce EMMPRIN. These findings show that EMMPRIN is increased in lung fibrosis.

Adolescent↗
PubMed1994

Lung transplantation for chemotherapy-induced pulmonary fibrosis.

A 26-year-old man cured of childhood acute lymphoblastic leukemia underwent a single lung transplant for drug-induced pulmonary toxicity 9 years after the completion of chemotherapy. It is not known whether patients cured of a malignancy who undergo organ transplantation are at increased risk of malignancy as compared to other organ transplant recipients. There was no evidence of recurrent or secondary malignancy in this case. Since single lung transplantation has been effective for idiopathic pulmonary fibrosis, it should be considered for patients cured of a malignancy who develop chemotherapy-induced pulmonary fibrosis.

Adult↗
PubMed1985

[Recent advances in the study of the mechanisms of silica-induced pulmonary fibrosis].

A review was made on the recent advances in the study on the pathogenesis of silica-induced pulmonary fibrosis. Alveolar macrophages which ingest silica particles liberate a fibrogenic factor, which stimulates the production of collagen of cultured fibroblasts. Silica deposited in the alveoli augments the demand of macrophages, the supply of which is maintained by monocytes recruited from the bone marrow. Attempts to demonstrate in vitro the presence of a fibrogenic factor in the supernatant of macrophages have been made in many laboratories, and an in vivo model utilizing diffusion chambers implanted in mice has been used by some investigators. A fibrogenic factor has been isolated and purified from the medium of silica-treated macrophages. Recent advances in immunological studies have demonstrated that silica stimulates macrophages to release monokines such as interleukin 1 (IL-1) and that IL-1 has chemical properties identical to the fibrogenic factor, which enhances the level of collagen production by modulating the proliferation of fibroblasts. Silica inhibits the suppressive effects of macrophages on fibroblasts. The increased protein synthesis in the fibroblasts is due partly to increase in mRNA. Collagen synthesis is stimulated not only by the fibrogenic factor released from silica-treated macrophages but also by the inhibition of macrophage ribonuclease activity. Information on the number of cells, collagen content and protease activity in the lung as well as in the bronchopulmonary lavage fluid has provided us a better understanding of the mechanisms involved in silica-induced pulmonary fibrosis.

Animals↗
PubMed2000

The potential role of PDGF, IGF-1, TGF-beta expression in idiopathic pulmonary fibrosis.

OBJECTIVE: To identify the role of cytokines involved in the development of lung fibrosis in patients with idiopathic-pulmonary fibrosis (IPF). METHODS: Proteins and gene expression of platelet-derived growth factor (PDGF)-A and -B, insulin-like growth factor 1 (IGF-1), and transforming growth factor beta (TGF-beta) were measured in alveolar macrophages and open lung biopsies from patients with IPF using immunohistochemistry (IHC) and in situ hybridization (ISH). RESULTS: In specimens of bronchoalveolar lavage fluid (BALF), PDGF-A, PDGF-B, IGF-1, TGF-beta were localized in alveolar macrophages. Evaluation of open lung biopsies from patients with IPF showed that IGF-1 was prominently present in pulmonary vessel walls in fibrotic lesions. PDGF and TGF-beta proteins were localized to hyperplastic bronchio-alveolar epithelial cells, alveolar macrophages, fibroblasts, vascular smooth muscle and endothelial cells. Our in situ hybridization results were consistent with that of immunohistochemistry except that PDGF-A and TGF-beta mRNA transcripts were not detected in bronchoalveolar epithelial cells. CONCLUSION: These observations suggest that (1) alveolar macrophages play key roles not only in inflammation but also in the fibrotic process by releasing PDGF, IGF-1 and TGF-beta; (2) IGF-1 could be responsible for angiogenesis in IPF; (3) PDGF, TGF-beta are associated with fibroplasia and the deposition of extracellular matrix, as well as vessel remodeling and epithelial cell repopularization.

Adult↗
PubMed1974

The pathogenesis of bleomycin-induced pulmonary fibrosis in mice.

Administration of 0.5 mg bleomycin to mice twice weekly for 4 weeks induced pulmonary fibrosis. The initial site of injury was the intima of pulmonary arteries and veins where endothelial cells became edematous and were separated from the underlying basement membrane by large blebs. These lesions occurred after 2 weeks and were associated with infiltration of perivascular spaces by lymphocytes and plasma cells. Capillary endothelial blebbing and interstitial edema were observed after 4 weeks, when multifocal necrosis of type 1 alveolar epithelial cells was accompanied by fibrinous exudation into the alveoli. The process of repair was characterized by proliferation and metaplasia of type 2 epithelial cells, fibroblastic organization of alveolar fibrin and fibrosis of the interstitium within 8 to 12 weeks. The consistent induction of changes similar to those of diffuse pulmonary fibrosis or fibrosing alveolitis in man suggests that bleomycin-induced injury may provide a suitable model for the investigation of this ill-defined group of diseases.

Animals↗
PubMed1995

Coronary artery revascularization followed by single-lung transplantation in a patient with combined end-stage idiopathic pulmonary fibrosis and left main coronary artery stenosis.

Single-lung transplantation has been used successfully in patients who have idiopathic pulmonary fibrosis; however, coronary artery disease is often considered a contraindication for lung transplantation in such patients. We report the case of a 53-year-old man with idiopathic pulmonary fibrosis in whom left main coronary artery stenosis was found incidentally during pretransplant evaluation. The patient was treated successfully with elective coronary artery bypass grafting, followed by left single-lung transplantation 35 days later.

Coronary Angiography↗
PubMed2002

The role of sodium cromolyn in treatment of paraquat-induced pulmonary fibrosis in rat.

Paraquat is a non-selective herbicide which is widely used in agriculture. It has potential of producing pulmonary fibrosis. In this study the therapeutic effect of different doses of sodium cromolyn on the development of paraquat-induced pulmonary fibrosis was investigated. In order to produce lung fibrosis, rats were given single oral dose of paraquat (40 mg kg(-1)). Two groups of animals were nebulised with 6 or 8 mg day(-1) cromolyn (divided into two doses per day) 5 days prior and 2 weeks after paraquat treatment. Control animals were given equivalent volume of normal saline and treated with cromolyn similar to the test groups. Rats were killed at the end of treatment course and lung tissues were tested histologically and biochemically. Histological examination of paraquat-treated animals showed marked infiltration of inflammatory cells in the alveolar spaces, septal thickening and fibrosis. Lesions were evident in many places of sections. Sodium cromolyn could markedly reduce such damages in lung tissue. Lung weight, hydroxyproline and collagen content of lung tissues were elevated significantly (P < 0.05) in paraquat group compared with control group. In cromolyn-treated groups such factors were near to control value and were significantly lower than paraquat group (P < 0.05). Results of this study indicate that sodium cromolyn can decrease the fibrogenic effect of paraquat on lung. Such effect may be due to the stabilising of mast cells and inhibition of inflammatory mediators by sodium cromolyn.

Animals↗
PubMed2004

[Relationship between bleomycin-induced pulmonary fibrosis and vascular endothelial cell injury].

OBJECTIVE: To explore the relationship between the injury of vascular endothelial cells and formation of lung fibrosis by bleomycin (BLM) in rats. METHODS: The rats of experimental groups were treated with bleomycin intratracheally to induce pulmonary fibrosis. The expression of vascular endothelial growth factor (VEGF) in pulmonary tissues were analyzed qualitatively and quantitatively by immunohistochemistry and image analysis system. RESULTS: (1) HISTOLOGY: Edema in rat alveoli and alveolar septum, inflammatory cells exudation, degeneration and necrosis of type I and type II alveolar epithelial cells (AETI and AETII), ruptured alveolar basement membrane, as well as swollen vascular endothelial cells and karyopyknosis were observed in 3 d and 7 d after treatment with BLM. AETII proliferation, with more fibroblasts in alveolar septum, and new capillary vessel formation in 7, 14 d, as well as thickened alveolar septum, damaged alveolar structure, and obvious pulmonary tissue fibrosis in 28 d after treatment with BLM were observed. (2) Immunohistochemistry: in normal control, VEGF expressed weakly in pulmonary tissue distributing mainly in AETII, bronchial epithelial cells, alveolar macrophages and leydig's cells. While in bleomycin treated groups, the expression of VEGF increased markedly. The expression in AETII, and pulmonary macrophage were significantly higher than that in control in 3 d to 28 d (P < 0.05, P < 0.01). The rat leydig's cells also had higher expression of VEGF in 7, 14, 28 d (P < 0.05, P < 0.01). CONCLUSION: The high expression of VEGF is related to vascular endothelial cells injury which may be one of important factors in the formation of bleomycin-induced pulmonary fibrosis.

Animals↗
PubMed2007

Towards systems biology of human pulmonary fibrosis.

The integrated effect of multiple pathways, molecules, genetic polymorphisms, environmental stimuli, and possible infection determines the lung phenotype in idiopathic pulmonary fibrosis (IPF), a chronic progressive and often lethal lung disease. Systems biology approaches aim to provide a systemwide view of biological process using computational tools and high-throughput technologies. Although much of the analysis of genome-level transcriptional high-resolution profiles of IPF was reductionist, usually focusing on a single factor in the disease process, there are some studies that implement systems approaches. We discuss these analyses and provide examples of the global analysis of IPF, hypersensitivity pneumonitis, and nonspecific interstitial pneumonia. Detailed quantitative phenotyping and correlation with microarray results as well as high-throughput genotyping should provide us with the datasets to implement systems biology approaches in fibrosis research. Interdisciplinary teams and training of junior investigators in the vocabulary of systems biology should allow us to use these datasets integratively and generate a global model of human pulmonary fibrosis.

Animals↗
PubMed1994

[The role of pulmonary macrophages in the development of pulmonary fibrosis caused by asbestos].

The role of alveolar and interstitial macrophages in asbestos-induced pulmonary fibrosis is discussed. Asbestosis is thought to result from a series of cellular interaction involving the pulmonary macrophages and lung fibroblasts. Inhaled asbestos fibres activate serum complement-dependent chemoattractant for macrophages which accumulate at alveolar duct bifurcations playing a central role in phagocytosis fibers and forming early pulmonary lesions. After phagocytic stimulation macrophages release various chemotactic factors for neutrophils and other inflammatory cells including TNF, neutrophil chemotactic factor and many proinflammatory mediators such as prostaglandins, leukotrienes, thromboxane. Apart from that, macrophages produce free radical oxygen and release lysosome enzymes which may cause lung tissue injury. There is also concomitant accumulation of fibroblasts proliferating in response to macrophages-derived growth factors, interleukin-1 and fibronectin. As a result of those processes collagen production increase and pulmonary fibrosis develops.

Animals↗
PubMed2003

Conditional expression of transforming growth factor-alpha in adult mouse lung causes pulmonary fibrosis.

To determine whether overexpression of transforming growth factor (TGF)-alpha in the adult lung causes remodeling independently of developmental influences, we generated conditional transgenic mice expressing TGF-alpha in the epithelium under control of the doxycycline (Dox)-regulatable Clara cell secretory protein promoter. Two transgenic lines were generated, and following 4 days of Dox-induction TGF-alpha levels in whole lung homogenate were increased 13- to 18-fold above nontransgenic levels. After TGF-alpha induction, transgenic mice developed progressive pulmonary fibrosis and body weight loss, with mice losing 15% of their weight after 6 wk of TGF-alpha induction. Fibrosis was detected within 4 days of TGF-alpha induction and developed initially in the perivascular, peribronchial, and pleural regions but later extended into the interstitium. Fibrotic regions were composed of increased collagen and cellular proliferation and were adjacent to airway and alveolar epithelial sites of TGF-alpha expression. Fibrosis progressed in the absence of inflammatory cell infiltrates as determined by histology, without changes in bronchiolar alveolar lavage total or differential cell counts and without changes in proinflammatory cytokines TNF-alpha or IL-6. Active TGF-beta in whole lung homogenate was not altered 1 and 4 days after TGF-alpha induction, and immunostaining was not increased in the peribronchial/perivascular areas at all time points. Chronic epithelial expression of TGF-alpha in adult mice caused progressive pulmonary fibrosis associated with increased collagen and extracellular matrix deposition and increased cellular proliferation. Induction of pulmonary fibrosis by TGF-alpha was independent of inflammation or early activation of TGF-beta.

Age Factors↗