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PubMed2005

[Dynamic changes of found in inflammatory zone 1 protein and mRNA expression in the lung with experimental pulmonary fibrosis of the rat.].

To investigate the role of found in inflammatory zone 1 (FIZZ1) protein in the pathogenesis of experimental pulmonary fibrosis, 48 male Sprague-Dawley rats were randomly divided into two groups, the pulmonary fibrosis group and the control group. Rat pulmonary fibrosis was reproduced by an intratracheal injection of bleomycin (5 mg/kg body weight). Normal saline (1 ml/kg body weight) was given intratracheally injection in the control group. There were 24 rats in each group, and 6 animals were separately killed on the 7th, 14th, 21th and 28th day after treated with bleomycin or normal saline. Then the following tests were undertaken: (1) HE and Masson staining of lung section;(2) Determination of lung tissue hydroxyproline (HYP);(3) Immunohistochemical staining of protein of FIZZ1 in the lung;(4) In situ hybridization of FIZZ1 mRNA in the lung. The results showed: (1) There were full of inflammatory cells in the lung, the interval of alveoli enlarged and many alveolar spaces disappeared on the 7th day after treated with bleomycin in the fibrosis group. Collagen began to proliferate after 14 d. The pulmonary fibrosis was stably established on the 28th day, full of green fibers in the Masson staining of lung section. (2) The expression of FIZZ1 protein in the lung increased after 7 d in bleomycin-treated animals (3.013+/-0.326 vs 0.473+/-0.056, P<0.01 vs control), but was slightly decreased on the 14th day (2.124+/-0.197) and expensively decreased on the 21st day (1.760+/-0.105) and the 28th day (0.691+/-0.081). (3) The expression of FIZZ1 mRNA in the lung also increased after 7 d by treated with bleomycin (3.795+/-0.338 vs 0.678+/-0.087, P<0.01 vs control), but decreased on the 14th day (1.276+/-0.104) and further decreased on the 28th day (0.896+/-0.084). The expression of FIZZ1 protein and mRNA in fibrosis group was higher than that in the control group (P<0.05 or P<0.01). The results suggest that FIZZ1 protein and FIZZ1 mRNA are dynamically changed in the lung with experimental pulmonary fibrosis, which may contribute to the pathogenesis of pulmonary fibrosis.

English Abstract↗
PubMed1996

Expression of immunoreactive activin A protein in remodeling lesions associated with interstitial pulmonary fibrosis.

The expression of activin A, one of the transforming growth factor-beta supergene family, was studied in various pulmonary conditions associated with interstitial pulmonary fibrosis (3 cases with diffuse alveolar damage, 6 cases with idiopathic pulmonary fibrosis, and 1 case with pulmonary fibrosis associated with rheumatoid arthritis) using immunohistochemical techniques on paraffin-embedded sections. Controls consisted of 10 cases with normal pulmonary parenchyma, and 2 cases with primary pulmonary hypertension and 1 case with secondary pulmonary hypertension were also studied. The lung specimens from normal parenchyma weakly expressed immunoreactive activin A on the bronchiolar epithelium. In marked contrast, all of the specimens from cases with diffuse alveolar damage and interstitial pulmonary fibrosis demonstrated strong expression of activin A on metaplastic epithelium, hyperplastic smooth muscle cells, desquamated cells, and alveolar macrophages. Pulmonary arteries from patients with primary or secondary pulmonary hypertension showed abundant immunoreactive activin A on smooth muscle cells. These findings suggest a potential role for this growth factor, activin A, in the pathogenesis of pulmonary tissue remodeling associated with interstitial pulmonary fibrosis.

Activins↗
PubMed1998

Differential expression of extracellular matrix remodeling genes in a murine model of bleomycin-induced pulmonary fibrosis.

Exposure to the chemotherapeutic drug bleomycin leads to pulmonary fibrosis in humans and has been widely used in animal models of the disease. Using C57BL/6 bleomycin-sensitive mice, pulmonary fibrosis was induced by multiple intraperitoneal injections of the drug. An increase in the relative amounts of steady-state alpha1(I) procollagen, alpha1(III) procollagen, and fibronectin mRNA as well as histopathological evidence of fibrosis was observed. The effect of bleomycin on the expression of the enzymes responsible for extracellular matrix degradation, the matrix metalloproteinases (MMPs), and their inhibitors (TIMPs), was selective and showed temporal differences during the development of fibrosis. Of the MMPs tested, bleomycin treatment resulted in the up-regulation of gelatinase A and macrophage metalloelastase gene expression in whole-lung homogenates, whereas gelatinase B, stromelysin-1, and interstitial collagenase gene expression was not significantly changed. Timp2 and Timp3, the murine homologues of the respective TIMP genes, were constitutively expressed, whereas Timp1 was markedly up-regulated during fibrosis. The strong correlation between enhanced extracellular matrix gene expression, differential MMP and TIMP gene expression, and histopathological evidence of fibrosis suggest that dysregulated matrix remodeling is likely to contribute to the pathology of bleomycin-induced pulmonary fibrosis.

Animals↗
PubMed1990

Idiopathic pulmonary fibrosis: can cell mediated immunity markers predict clinical outcome?

Most of the cells found in lung parenchyma in patients with idiopathic pulmonary fibrosis are activated T lymphocytes and macrophages. The serum levels of three markers of cell mediated immunity were measured in 20 patients with idiopathic pulmonary fibrosis, in 20 normal subjects and in 12 patients with sarcoidosis to evaluate their clinical and prognostic significance in idiopathic pulmonary fibrosis. The three markers were: soluble CD8 (from activated suppressor-cytotoxic lymphocytes), soluble interleukin (IL)-2 receptors (from activated T cells and macrophages), and neopterin (from activated macrophages). Patients with idiopathic pulmonary fibrosis had higher levels of all three markers than the control subjects. Soluble IL-2 receptor and neopterin tended to be lower (though not significantly) in patients with idiopathic pulmonary fibrosis than in those with sarcoidosis, whereas soluble CD8 was similar in the two groups of patients. No correlation was found between soluble IL-2 receptors or soluble CD8 and the clinical, radiological, and physiological measures of disease activity or with clinical outcome (after a mean follow up of 23 months). Tumour necrosis factor levels were also determined. Only 30% of patients with idiopathic pulmonary fibrosis or sarcoidosis had detectable circulating tumour necrosis factor; these patients had a lower percentage of bronchoalveolar lavage fluid neutrophils in their lavage fluid. Tumour necrosis factor levels did not correlate with clinical measures of severity or outcome. Thus our data support the hypothesis that cell mediated alveolitis occurs in idiopathic pulmonary fibrosis. They do not, however, provide evidence to support the use of these markers of cell mediated immunity to monitor the clinical course in these patients.

Adult↗
PubMed1980

Bleomycin-induced pulmonary fibrosis in the rat. Prevention with an inhibitor of collagen synthesis.

Pharmacologic treatment of pulmonary fibrosis has been limited to the use of corticosteroids occasionally combined with other immunosuppressive agents. We tested the ability of a proline analogue that is a potent inhibitor of collagen biosynthesis to prevent the manifestations of bleomycin-induced pulmonary fibrosis in an animal model. Bleomycin sulfate was administered by intratracheal instillation to produce pulmonary fibrosis in male Fischer 344 rats. After 28 days lungs from bleomycin-treated animals had histologic, biochemical, and functional alterations consistent with pulmonary fibrosis. Vital capacity and compliance were reduced to 62% and 41% of their respective control values. Lung prolyl hydroxylase activity doubled during the first week after bleomycin, at a time when total lung collagen content remained unchanged. Thereafter total lung collagen content slowly rose to 72% above control values at 28 days. We administered the proline analogue DHP at a dose that completely inhibited the elevated levels of lung prolyl hydroxylase activity. Pulmonary collagen content of animals treated with DHP was only minimally elevated, and functional abnormalities were reduced. Pulmonary compliance increased significantly from 0.25 to 0.44 ml/cm of H2O, and vital capacity increased from 3.94 to 5.65 ml. These studies suggest that proline analogues offer potential for modifying the manifestations of pulmonary fibrosis that occur as a consequence of acute lung injury. Elevation of lung prolyl hydroxylase activity is an early even that serves as a useful index of the acute lung injury produced by bleomycin.

Animals↗
PubMed1980

Chronic obstructive pulmonary disease following idiopathic pulmonary fibrosis.

The rapid development of irreversible airflow obstruction in two nonsmoking women who recovered from acute idiopathic pulmonary fibrosis is discussed. Pulmonary fibrosis was diagnosed clinically and by lung biopsy. Recovery both clinically and radiologically was complete. Several pulmonary function studies in both patients showed a typical restrictive pattern (reduced lung volumes and carbon dioxide diffusing capacity, normal FEV1/FVC ratio). Within one year both patients exhibited an obstructive pattern of dysfunction (hyperinflation, gas trapping, reduced airflow measurements). These patients illustrated irreversible airway obstruction following recovery from the restrictive stage of pulmonary fibrosis.

Airway Resistance↗
PubMed1998

Comparison of the functional results of single lung transplantation for pulmonary fibrosis and chronic airway obstruction.

BACKGROUND: Single lung transplantation (SLT) is now a treatment option for patients with both pulmonary fibrosis and advanced chronic airway obstruction. Lung function after transplantation might be expected to be different in these two groups of patients because of the effect of the remaining native lung, but the implications of these differences have not been fully explored. METHODS: The functional results of a stable population of 20 patients (13 chronic airway obstruction, seven pulmonary fibrosis) after SLT with no evidence of obliterative bronchiolitis were analysed. The differences between the two populations in the interrelations between and determinants of total lung capacity (TLC), subdivisions of lung volume, airway function (spirometry, maximum expiratory flow volume curves, and moments analysis of the spirogram) respiratory mechanics (PV curves and maximal respiratory pressures), CO transfer factor (TLCO) and the distribution of perfusion, ventilation and volume of the transplanted and native lungs were compared. RESULTS: Total lung capacity after SLT (TLCpost) was normal in the patients with pulmonary fibrosis (mean (SE) 103.9 (6.9)% predicted) but remained significantly elevated in patients with airway obstruction (126.4 (4.4)%. Forced expiratory volume in one second (FEV1) and vital capacity (VC) improved to similar values after SLT in both groups with a final VC of 76.8 (5.9)% and 66.7 (3.9)% in patients with fibrosis and airway obstruction, respectively. Maximum expiratory flows were generally lower and moments analysis of the spirogram showed slower lung emptying with significantly greater second and third moments (alpha 2 and alpha 3) in patients with airway obstruction. Relative ventilation and perfusion of the transplanted lung were both greater in both populations but relative ventilation of the transplanted lung was significantly greater in patients treated for airway disease than in those with pulmonary fibrosis. TLCO was also significantly higher in patients who had received a transplant for chronic airway obstruction. CONCLUSIONS: These results suggest that differences in the functional results of SLT for airway disease and pulmonary fibrosis are relatively minor. In this series the native hyperinflated lung in chronic airway disease was not more disadvantageous to overall function than the native lung in pulmonary fibrosis. However, tests of lung function based on the terminal portion of the forced spirogram are likely to be less sensitive for the detection of obliterative bronchiolitis in patients who have received a transplant for advanced airway obstruction than in those with pulmonary fibrosis.

Female↗
PubMed2000

Role of carbohydrate antigens sialyl Lewis (a) (CA19-9) in bronchoalveolar lavage in patients with pulmonary fibrosis.

BACKGROUND: It has been reported that carbohydrate antigen sialyl Lewis (a) (CA19-9) levels are elevated in serum as well as in bronchoalveolar lavage fluid (BALF) of patients with pulmonary fibrosis. However, the biological significance of CA19-9 is unclear. OBJECTIVE: The purpose of the present study was to evaluate correlations between CA19-9 levels in BALF and several biochemical as well as clinical parameters in patients with pulmonary fibrosis. In addition, biological functions of CA19-9 were also examined. METHODS: We studied 24 patients with a diagnosis of pulmonary fibrosis: 16 with idiopathic pulmonary fibrosis (IPF) and 8 with pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD). In BALF, carbohydrate antigens sialyl Lewis (a) (CA19-9), elastase: alpha(1)-proteinase inhibitor complex (E-PI), hepatocyte growth factor (HGF), LDH, IgG, IgA, albumin, and cell differentiation were measured. We also evaluated the effects of CA19-9 on neutrophil functions. RESULTS: CA19-9/albumin levels in BALF significantly correlated with HGF/albumin, elastase/albumin, LDH/albumin, total number of alveolar macrophages, and total number of neutrophils. Purified CA19-9 had a chemotactic activity for neutrophils. In addition, neutrophil chemotactic activity to C5a, fMLP, and interleukin 8 was significantly stimulated after incubation with purified CA19-9. Furthermore, CA19-9 increased the expression of CD15s on neutrophils. CONCLUSIONS: Our data demonstrated (i) CA19-9 in BALF correlated with other markers of inflammation in pulmonary fibrosis, and (ii) CA19-9 can modify neutrophil functions. These results suggest that CA19-9 may play a role in the process of lung injury in patients with pulmonary fibrosis.

Adult↗
PubMed1998

Immunohistochemical localisation of advanced glycation end products in pulmonary fibrosis.

AIM: To investigate the presence and distribution of advanced glycation end products (AGE) in pulmonary fibrosis. METHODS: Lung tissue samples obtained from seven necropsy cases with idiopathic pulmonary fibrosis and seven with normal pulmonary parenchyma were examined immunohistochemically with a monoclonal antibody specific for AGE: 6D12. We also tested three cases with diffuse alveolar damage. RESULTS: All the specimens from cases with pulmonary fibrosis and diffuse alveolar damage showed strong AGE expression on macrophages. Lung specimens from normal parenchyma showed positive AGE immunoreactivity on macrophages from only two of seven cases. CONCLUSIONS: These findings suggest that AGE modified proteins accumulate in alveolar macrophages in patients with diffuse alveolar damage and idiopathic pulmonary fibrosis.

Aged↗
PubMed1994

Partial reversal of established bleomycin-induced pulmonary fibrosis by rh-urokinase in a rat model.

Pulmonary fibrosis was induced in male Sprague-Dawley rats by intratracheal instillation of bleomycin. By 30 d post-bleomycin, the lungs exhibited elevated interstitial collagen levels. Thirty d after exposure to bleomycin, animals were further treated by intratracheal administration of phosphate-buffered saline (PBS) or 12,500 units of recombinant human urokinase (rh-UK). Three days later, the animals were sacrificed and the lungs fixed, sectioned, and assessed for fibrosis. The presence of interstitial collagen was quantitated using a BioQuant Image Analysis System (R and M Biometrics, Inc., Nashville, TN). Urokinase treatment of animals with established pulmonary fibrosis induced by exposure to 0.5 units of bleomycin was found to diminish the collagen content of lungs to near control levels by 3 d post-UK treatment. By 36 d post-UK treatment (66 d post-bleomycin), values for interstitial collagen were again partially elevated, indicating that UK treatment interfered with established fibrosis but did not stop the bleomycin-mediated process. However, the extent of fibrosis was less than that observed in lungs from non-UK treated animals 66 d post-bleomycin. UK treatment initiated 63 d post-bleomycin exposure again revealed a decline in the extent of fibrosis, but the values did not return to baseline levels. A repeat of the short-term experiment with a higher dose of bleomycin (0.85 units) again revealed that UK treatment was effective in diminishing the extent of fibrosis from 22% to 12% collagen. These results indicate that exogenous UK may be an effective therapeutic modality in the treatment of pulmonary fibrosis induced by some stimuli or developing in association with diseases such as scleroderma.

Animals↗
PubMed2006

Idiopathic pulmonary fibrosis related to endothelial injury and antiendothelial cell antibodies.

Mechanisms underlying idiopathic pulmonary fibrosis are not well understood. This paper presents data supporting the hypothesis that microvascular endothelial cell injury and antiendothelial cell antibodies play roles in human idiopathic pulmonary fibrosis. Serologic and pathologic features of 40 patients diagnosed with idiopathic pulmonary fibrosis were evaluated. All patients had open lung biopsies indicating either usual or nonspecific interstitial pneumonitis. All biopsies had morphologic evidence of microvascular injury to the endothelium, and direct immunofluorescence testing revealed variable deposition of IgG, IgM, or IgA within septal microvasculature suggestive of humorally mediated microvascular injury. Ultrastructural studies revealed changes of endothelial cell injury and necrosis and evidence of repetitive episodes of microvascular injury characterized by basement membrane zone collagen deposition and lamellation. Serum samples demonstrated reactivity to multiple endothelial cell antigenic epitopes, and indirect immunofluorescent testing demonstrated a prominent pattern of fluorescence in pulmonary endothelial cell preparations. Serum samples were positive in 37/40 patients for antiphospholipid antibodies with one fourth having positive lupus anticoagulant tests accompanied by thrombotic episodes. In patients with idiopathic pulmonary fibrosis, Factor VIII levels and C-reactive protein levels were also elevated, supporting the presence of endothelial cell injury and inflammation. These data underscore a potential role for immune-based microvascular injury in the evolution of usual or nonspecific interstitial pneumonitis and indicate that those patients have evidence of microvascular injury and endothelial cell necrosis. The high prevalence of antiphospholipid antibodies in these patients may lead to an inherent thrombophilic tendency.

Adult↗
PubMed2002

Effects of tamoxifen on pulmonary fibrosis after cobalt-60 radiotherapy in breast cancer patients.

BACKGROUND AND PURPOSE: This study was performed to investigate whether the tamoxifen (TAM) induced the development of pulmonary fibrosis after post-mastectomy cobalt-60 (Co-60) irradiation of chest wall and regional lymphatics in patients with breast cancer along with patient age, menopausal status, body weight, observation time and adjuvant chemotherapy regimens. MATERIALS AND METHODS: In this prospective study, 74 patients treated with post-mastectomy adjuvant radiotherapy (RT) and TAM and 37 patients treated with RT were evaluated by axial computerized tomography (CT). CT was first performed before initiation of radiotherapy and TAM treatment. A total of 824 thorax CT sections were evaluated by a radiologist blindly. Comparison of pre-treatment and post-treatment CT sections was used to monitor the development of pulmonary fibrosis. RESULTS: Pulmonary fibrosis developed in 26 of 74 patients who were treated with RT and TAM combination. It was found in five of 37 women treated only with RT. The difference was statistically significant (P<0.01). The median time for the development of pulmonary fibrosis was 8 months in TAM-treated patients whereas it was 10 months in non-TAM-treated patients. Among 111 patients who participated in that study, 65 were in the post-menopausal state and 46 in pre-menopausal state. In the multivariate analysis, the independent prognostic factors were age (P=0.010) and menopausal status (P=0.019). Advanced age and post-menopausal status predisposed to pulmonary fibrosis. The time interval in the development of lung fibrosis and body weight did not significantly influence the results. The time interval which is one independent prognostic factor was found to be associated with lung fibrosis under only-RT group in multivariate analysis (P<0.01). CONCLUSION: TAM treatment during post-mastectomy RT in breast cancer patients significantly increases the risk of the development of lung fibrosis along with the patient age and menopausal status.

Age Factors↗
PubMed1986

Comparison of right ventricular weight at necropsy in interstitial pulmonary fibrosis and in chronic bronchitis and emphysema.

The ventricular weights in 43 patients with interstitial pulmonary fibrosis were retrospectively compared with those in 172 patients with emphysema and chronic bronchitis. The mean right ventricular weight of patients with interstitial pulmonary fibrosis and those with emphysema and chronic bronchitis was 85.5 g (SD 23.2) and 88.8 g (34.3), respectively. Thirty five patients (81%) with interstitial pulmonary fibrosis had a right ventricular weight over 65 g compared with 124 (72%) of those with emphysema. Fifty three per cent of both those with interstitial pulmonary fibrosis and those with chronic bronchitis and emphysema had a right ventricular weight greater than 80 g. Differences between the two groups were not significant. These results suggest that the prevalence of right ventricular hypertrophy and pulmonary hypertension in interstitial pulmonary fibrosis is similar to that found in chronic bronchitis and emphysema.

Aged↗
PubMed2005

[Cell apoptosis and the change of Fas/FasL gene in experimental pulmonary fibrosis].

OBJECTIVE: To investigate the changes and significance of cell apoptosis and Fas/FasL gene in pulmonary fibrosis. METHODS: Forty mice were divided into two groups randomly, each group contained twenty mice. TUNEL, immunohistochemistry and in situ hybridization were used to detect the change of cell apoptosis, Fas/FasL mRNA and protein in mice with pulmonary fibrosis caused by bleomycin. RESULTS: The apoptosis index of lung cells in the pulmonary fibrosis group (55.3 +/- 12.2) was higher than that of control group (4.7 +/- 1.0, t = 13.06, < 0.01). The expression of Fas/FasL mRNA (175.8 +/- 21.6, 5.2 +/- 1.6) and protein (956 +/- 96, 285 +/- 76) in the pulmonary fibrosis group was higher than that of control group (mRNA: 26.6 +/- 1.9, 0.5 +/- 0.4, t = 21.7, 8.79, all < 0.01; protein: 491 +/- 96, 100 +/- 18, t = 5.03, 12.81, < 0.01). CONCLUSION: The apoptosis index of lung cells, Fas/FasL genes and protein were up-regulated in lung tissue of pulmonary fibrosis, which may play an important role in the development of disease.

Animals↗
PubMed1999

In vivo gene transfer of an extracellular domain of platelet-derived growth factor beta receptor by the HVJ-liposome method ameliorates bleomycin-induced pulmonary fibrosis.

A number of investigators have reported augmented expression of PDGF in lungs with idiopathic pulmonary fibrosis (IPF) or with other types of pulmonary fibrosis. To accomplish such a regulation of PDGF activity, we constructed an expression plasmid of the extracellular domain of PDGF receptor beta chain (XR), which lacks intracellular tyrosine kinase domain and transmembrane portions, and estimated the therapeutic effects of XR gene transfer through the trachea on bleomycin-induced lung fibrosis of C57BL/6 mice using the hemagglutinating virus of Japan(HVJ)-liposome method. The XR gene transfer ameliorated the increases in the wet weight and hydroxyproline content and the histopathologic changes of the lung induced by bleomycin. These findings suggest that PDGF plays a crucial role in the pathogenesis of pulmonary fibrosis, and that XR gene transfer using the HVJ-liposome method may limit the progression of pulmonary fibrosis.

Animals↗
PubMed1997

Pulmonary fibrosis associated with polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) and exacerbated pulmonary fibrosis presented concurrently in a 69-year-old woman with a 5-year history of idiopathic interstitial pneumonia. The radiographic and histological examinations suggested usual interstitial pneumonia (UIP) as a more likely diagnosis. Corticosteroid therapy resulted in relief of the patient's muscle symptoms and improvement in the functional and radiographical signs of the pulmonary fibrosis. The final diagnosis was pulmonary fibrosis associated with PMR, because PMR is believed to be one of the causes contributing to interstitial lung diseases.

Aged↗
PubMed2003

Overexpression of tumor necrosis factor-alpha diminishes pulmonary fibrosis induced by bleomycin or transforming growth factor-beta.

Tumor necrosis factor-alpha (TNF-alpha) is thought to be important in the development of pulmonary fibrosis. However, surfactant protein-C/TNF-alpha transgenic mice do not spontaneously develop pulmonary fibrosis but instead develop alveolar enlargement and loss of elastic recoil. We hypothesized that overexpression of TNF-alpha in the lung requires an additional insult to produce fibrosis. In this study we evaluated whether TNF-alpha overexpression altered the development of pulmonary fibrosis due to bleomycin or transforming growth factor-beta (TGF-beta). Either 0.2 U bleomycin or saline was administered into left lung of TNF-alpha transgenic mice and their transgene-negative littermates. To overexpress TGF-beta, an adenovirus vector containing either active TGF-beta (AdTGF-beta) or LacZ was administered at a dose of 3 x 108 plaque-forming units per mouse. Fibrosis was assessed histologically and by measurement of hydroxyproline. TNF-alpha transgenic mice tolerated bleomycin or AdTGF-beta, whereas the transgene-negative littermates demonstrated severe pulmonary fibrosis after either agent. An increase in prostaglandin E2 and downregulation of TNF receptor I expression were observed in the TNF-alpha transgenic mice. In addition, recombinant human TNF-alpha attenuated bleomycin-induced pulmonary fibrosis. TNF-alpha has a complex role in the development of pulmonary fibrosis. Endogenous TNF-alpha may be important in the development of fibrosis as indicated in other reports, but overexpression of TNF-alpha or exogenous TNF-alpha limits pulmonary fibrosis in mice.

Adenoviridae↗