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PubMed2004

Th1 cytokine pattern (IL-12 and IL-18) in bronchoalveolar lavage fluid (BALF) before and after treatment with interferon gamma-1b (IFN-gamma-1b) or colchicine in patients with idiopathic pulmonary fibrosis (IPF/UIP).

BACKGROUND AND AIM: Characterization of the biologic effects of Th1 cytokines will enhance the understanding of idiopathic pulmonary fibrosis (IPF) pathogenesis and treatment selection. Th1 response is characterized by increased expression of IFN-gamma, interleukin (IL)-12 and IL-18. The present study aims to evaluate the role of Th1 cytokines and their possible changes in the bronchoalveolar lavage fluid (BALF), before and after treatment with IFN-gamma-1b or colchicine. PATIENTS AND METHODS: We studied prospectively 10 patients (8 male, 2 female) of median age 67 yr with histologically confirmed IPF/UIP. Patients were randomly assigned to receive either IFN-gamma-1b 200 microg sc (5 patients) or colchicine 1 mg qd (5 patients) plus prednisone 10 mg qd. BALF IL-12 and IL-18 levels were measured before and after treatment. RESULTS: BALF IL-12 levels before and after treatment did not differ significantly between the two treatment groups. However, BALF IL-18 levels were significantly decreased after treatment with IFN-gamma-1b (mean +/- SD, 58.4 +/- 15.6 pg/mL vs 42.8 +/- 4.90 pg/mL, p < 0.05). A significant difference was also found after treatment with colchicine (mean +/- SD, 66.8 +/- 36.9 pg/mL vs 42.6 +/- 1.08 pg/mL, p < 0.01). A significant correlation was found between IL-18 BALF levels and the BALF neutrophils (r = 0.75, p = 0.024). CONCLUSION: Our data suggest the potential role of IL-18 as an inflammatory marker in the pathogenetic pathway of IPF such as its possible downregulation by IFN-gamma-1b treatment. Further studies are needed in a higher number of patients in order to define the precise role of both cytokines during the immunoregulatory response with IFN-gamma-1b.

Aged↗
PubMed2006

In vitro tracheal hyperresponsiveness to muscarinic receptor stimulation by carbachol in a rat model of bleomycin-induced pulmonary fibrosis.

1 Bleomycin-induced lung injury is widely used as an experimental model to investigate the pathophysiology of pulmonary fibrosis but the alterations in the pharmacological responsiveness of airways isolated from bleomycin-exposed animals has been scarcely investigated. The aim of this study was to examine the in vitro tracheal responses to muscarinic receptor stimulation with carbachol in a rat bleomycin model. 2 Concentration-response curves to carbachol (10 nm to 0.1 mm) were obtained in tracheal rings isolated from Sprague-Dawley rats 14 days after endotracheal bleomycin or saline. The intracellular calcium signal in response to carbachol (10 microm) was measured by epifluorescence microscopy using fura-2 in primary cultures of tracheal smooth muscle cells from bleomycin- and saline-exposed rats. Circulating plasma tumour necrosis factor (TNF)-alpha/interleukin (IL)-1beta levels were measured by enzyme-linked immunosorbent assay. 3 Maximal contraction in response to carbachol was significantly greater in tracheal rings from bleomycin-exposed rats compared with controls (15.8 +/- 1.3 mN vs. 11.8 +/- 1.4 mN; n = 19, P < 0.05). 4 Carbachol (10 microm) elicited a transient increase of intracellular calcium with greater increment in tracheal smooth muscle cells from bleomycin-exposed rats compared with controls (372 +/- 42 nmvs. 176 +/- 20 nm; n = 7, P < 0.01). 5 Circulating plasma levels of TNF-alpha/IL-1beta were augmented in bleomycin-exposed rats compared with controls. Tissue incubation with TNF-alpha (100 ng ml(-1))/IL-1beta (10 ng ml(-1)) increased in vitro tracheal responsiveness to carbachol. 6 In conclusion, tracheal contraction in response to muscarinic receptor stimulation with carbachol was increased in bleomycin-exposed rats. This in vitro cholinergic hyperresponsiveness may be related to the augmented levels of inflammatory cytokines in bleomycin-exposed rats.

Animals↗
PubMed1999

Treatment of bleomycin-induced pulmonary fibrosis by transfer of urokinase-type plasminogen activator genes.

During acute and chronic inflammatory lung diseases, the normal fibrinolytic activity in the alveolar space is inhibited by increased levels of plasminogen activator inhibitor 1 (PAI-1). Transgenic mice having increased fibrinolytic activity due to genetic deficiency of PAI-1 develop less fibrosis after bleomycin-induced lung inflammation. These observations led us to hypothesize that pulmonary fibrosis could be limited through enhancement of alveolar fibrinolytic activity by adenovirus-mediated transfer of the urokinase-type plasminogen activator (uPA) gene to the lung. To investigate this hypothesis, 0.075 U of bleomycin was introduced intratracheally into mice. Twenty-one days later, the mice were treated intratracheally with phosphate-buffered saline (PBS), a control adenovirus, or adenoviruses containing murine or human uPA cDNAs. On day 28, the mice were sacrificed, and lung fibrosis was quantitated by measuring hydroxyproline content. As expected, bleomycin caused a doubling in lung hydroxyproline to 345.6+/-28.2 microg/lung (SEM) compared with mice receiving PBS (170.2+/-4.0 microg/lung). Treatment of the bleomycin-injured mice with the control adenovirus on day 21 had no impact on lung fibrosis (338.4+/-17.2 microg/lung). Importantly, the human uPA adenovirus significantly reduced (p<0.05) lung hydroxyproline (281.2+/-22.8 microg/lung), thus attenuating by 38% the bleomycin-induced increase in lung collagen. The improvement in bleomycin-induced lung fibrosis resulting from treatment with the human uPA adenovirus further supports the importance of the fibrinolytic system during inflammatory lung injury and repair.

Adenoviridae↗
PubMed1981

[Three new cases of pulmonary fibrosis in finishers of tools reinforced with tungsten carbide (author's transl)].

On the basis of three new cases of pulmonary fibrosis due to heavy metals, the authors review the various clinical, radiological and respiratory function test criteria which lead to the diagnosis of this type of occupational fibrosis. This is an uncommon disease (21 cases published up to the present in France), insufficiently known, but with significant and sometimes severe risks. On July 19th 1980, the disease was added to the list of occupational diseases with No 70.

Adult↗
PubMed1987

Pulmonary fibrosis in rheumatoid arthritis: a review of clinical features and therapy.

During the past four decades there has been a growing appreciation of the frequency of pulmonary abnormalities associated with RA. Approximately 30% to 40% of patients with RA demonstrate either radiographic or pulmonary function abnormalities indicative of interstitial fibrosis or restrictive lung disease. The severity of pulmonary fibrosis is not associated with rheumatologic symptoms or the duration of the associated RA, nor is there any clear relation to the extraarticular features of RA or serologic findings. Survival rates in patients with coexisting RA and pulmonary fibrosis are similar to those of patients with idiopathic pulmonary fibrosis. However, the spectrum of disease activity is quite variable. The majority of patients with progressive pulmonary symptomatology, when treated with corticosteroids, will have equivocal results. Some patients appear to respond to immunosuppressive or cytotoxic medications. The role of macrophages may be central to the injury to lung. Recent studies suggest a potential treatment role for cyclosporine, which may be able to interrupt lymphocyte-stimulated macrophage activation, and thus, fibroblast-mediated fibrosis in patients with pulmonary interstitial fibrosis. Bronchoalveolar lavage studies may delineate subgroups of patients who are more likely to respond to immunosuppressive agents, especially when treatment is started early.

Adrenal Cortex Hormones↗
PubMed2004

Cyclooxygenase-2 is up-regulated in lung parenchyma of chronic obstructive pulmonary disease and down-regulated in idiopathic pulmonary fibrosis.

BACKGROUND AND AIM OF THE WORK: In vitro studies have suggested that fibroblasts from idiopathic pulmonary fibrosis (IPF) may have an impaired induction of cyclooxygenase (Cox)-2. We have investigated Cox-1 and Cox-2 expression in lung tissue from IPF. METHODS: Cox-1 and Cox-2 expression were determined using RT-competitive PCR and immunohistochemistry in pulmonary biopsies from IPF (n = 22), chronic obstructive pulmonary disease (COPD) (n = 13), and lung tissue from subjects undergoing pleurodesis for spontaneous pneumothorax (control group, n = 17). RESULTS: Immunohistochemical analysis showed that the score of Cox-2 positive cells was higher in COPD (1 +/- 0) with respect to fibrosis (0.37 +/- 0.1, p < 0.05) and controls (0.57 +/- 0.2). There were no differences between fibrosis and controls in Cox-2 positive cells. The expression of Cox-2 mRNA was significantly higher in COPD (3.26 +/- 0.72 x 10(6) molecules cDNA/microg total RNA) in comparison to IPF (0.57 +/- 0.17) and controls (0.54 +/- 0.16) (p < 0.001). After IL-1beta stimulation (1-10 ng/ml) Cox-2 mRNA basal expression increased significantly in controls (from 35 +/- 12 to 94 +/- 4 x10(6) molecules cDNA/microg total RNA, p < 0.01) and in COPD (from 38 +/- 8 to 92 +/- 3, p < 0.01). In contrast, no significant changes in Cox-2 mRNA expression were found in IPF (from 30 +/- 12 to 43 +/- 16). CONCLUSIONS: Our results suggest that differences in Cox-2 expression may play a role in the regulation of inflammatory responses in lung diseases. Excessive activity is associated with the development of chronic obstructive lung disease, while a limited activation following pro-inflammatory stimulation might contribute to fibrogenic responses.

Adult↗
PubMed2006

An ill wind-iatrogenic air embolus around pacing leads during defibrillator implant with coexisting pulmonary fibrosis.

We present a case of air embolism during biventricular defibrillator implantation in a 58-year-old man with pulmonary fibrosis. To prevent air entry after the dilator was removed, the subclavian venous sheath was covered before the lead was introduced. Air embolism occurred during inspiration around the lead body in the appropriate sized sheath but without a hemostatic valve. Extraordinary swings in intrathoracic pressure due to noncompliant lungs may have contributed to this unusual complication.

Defibrillators, Implantable↗
PubMed1998

Pulmonary fibrosis correlates with duration of tissue neutrophil activation.

The role of inflammatory cells such as neutrophil granulocytes in the pathogenesis of pulmonary scarring is unclear. We determined the metabolic activity of neutrophils with positron emission tomography (PET) to measure regional uptake of (18F)-2-fluoro-2-deoxy-D-glucose (18FDG) following its intravenous injection. Fibrogenic or nonfibrogenic substances were instilled into the right upper lobe of rabbit lungs. Time course and intensity of the 18FDG signal in the affected region varied markedly, depending on the stimulus. Time to peak signal (Tmax) and rate constant for its decline (k) for the test substances were, respectively: C5a 10 h (Tmax), 0.045 +/- 0.030 h-1 (k); Streptococcus pneumoniae 15 h, 0.068 +/- 0.012 h-1; bleomycin 28 h, 0.002 +/- 0.001 h-1; microcrystalline silica (microXSiO2), 90 h, 0.0012 +/- 0.0007 h-1; amorphous silica (aSiO2), no response. Response to the nonfibrogenic agents C5a, S. pneumoniae and aSiO2 was brief or nonexistent, falling to baseline values within 3 d, whereas that to the fibrogenic agents bleomycin and microXSiO2 persisted for up to 4 wk. Neutrophil numbers in the lung were proportional to the 18FDG signal following C5a and S. pneumoniae, but not bleomycin and microXSiO2. Autoradiography of lungs following administration of (3H)-deoxyglucose [(3H)-DG] showed specific localization to neutrophils in all models. Thus, 18FDG uptake provides a remarkably specific measure of neutrophil activity in situ, and the development of pulmonary fibrosis may be related to persistence of this activity.

Animals↗
PubMed1994

In situ hybridization analysis of rat lung alpha 1(I) and alpha 2(I) collagen gene expression in pulmonary fibrosis induced by endotracheal bleomycin injection.

BACKGROUND: Endotracheal bleomycin administration in rats and other animal species causes rapid development of pulmonary fibrosis, characterized by a transiently increased number of contractile, filament-laden parenchymal cells and increased lung collagen synthesis and deposition. However, the identity and source of the cells that actively synthesize collagen and other extracellular matrix and their relationship to the altered lung structure and function remain uncertain. EXPERIMENTAL DESIGN: In this study, the cells expressing alpha 1(I) and alpha 2(I) procollagen genes were identified and their localization analyzed in control and bleomycin-treated rat lungs at different time points, by in situ and Northern hybridization analyses. RESULTS: In control lungs, only a few scattered fibroblasts with weak expression of the alpha 1(I) procollagen gene were localized exclusively in the adventitia of the primary and tertiary bronchi, as well as major blood vessels. At day 3 after bleomycin treatment, scattered interstitial cells with significantly increased alpha 1(I) and alpha 2(I) procollagen gene expression were observed in the adventitia of bronchioles, terminal bronchioles, and adjacent small blood vessels. At days 7 and 14, there was a dramatic increase in the number of interstitial cells expressing large amounts of alpha 1(I) procollagen messenger RNA in these areas and extending to the lung parenchyma. This was followed on days 21 and 28 by significant decreases in procollagen gene expression and the number of cells with increased collagen gene expression. Most of the cells with enhanced collagen gene expression were arrayed in a disorganized fashion and were localized mainly around bronchioles, terminal bronchioles, and adjacent small blood vessels as well as in the irregularly distributed fibrotic foci, some submesothelial areas, and injured parenchyma. Northern blot analysis was consistent with the above in situ hybridization observation of the kinetics of collagen gene expression. CONCLUSIONS: The results indicate that in this rat fibrosis model, increased numbers of the interstitial cells with high expression of type I procollagen genes are derived primarily from the fibroblasts in the adventitia of bronchioles, terminal bronchioles, and adjacent blood vessels, as well as the submesothelial region. This then can result in further expansion to adjacent parenchyma and alveolar areas.

Animals↗
PubMedDate not supplied

Acute spontaneous pneumomediastinum in a child with Hodgkin's disease and pulmonary fibrosis.

A case of acute spontaneous pneumomediastinum in a 13-year-old boy suffering from Hodgkin's disease and pulmonary fibrosis is reported. He was initially treated for Pneumocystis carinii but his respiratory function progressively deteriorated, and fibrosis secondary to bleomycin was suspected. The day before the admission to the Pediatric Intensive Care Unit the patient complained of anterior thoracic pain, and a chest x-ray revealed a left-sided small spontaneous pneumothorax and pneumomediastinum. Although air leak responded initially to conservative treatment, acute tension pneumomediastinum with cardiopulmonary decompensation recurred 6 days later, while the patient was on mechanical ventilation. Treatment with urgent evacuation of the accumulated air via subxiphoid drainage, using an old but ill-defined technique, resulted in complete resolution of pneumomediastinum and significant improvement of the hemodynamic condition.

Acute Disease↗
PubMed2000

[Changes on the protein kinase C activity of alveolar macrophages in patients with idiopathic pulmonary fibrosis].

OBJECTIVE: To study the changes on protein kinase C(PKC) activity of alveolar macrophages (AM) in patients with idiopathic pulmonary fibrosis(IPF). METHOD: The PKC activity of AM in 9 healthy volunteers and 15 patients with IPF was investigated by radioactivity measuring. RESULTS: The total, cytosolic and particulate fraction PKC activity of AM in bronchoalveolar lavage fluid(BALF) from patients with IPF were higher than those from control group(P < 0.01 and P < 0.05). The total and the membrane fraction PKC activity had positive correlation with the number of cells in BALF(r = 0.8135, P < 0.01 and r = 0.5917, P < 0.05) respectively. CONCLUSION: As a bypass of transmembrane signal transduction, PKC was suggested to be involved in the development of IPF.

Adult↗
PubMed2001

Increased activity of protein kinase C in alveolar macrophages in idiopathic pulmonary fibrosis.

OBJECTIVE: To investigate the changes on protein kinase C (PKC) activity of alveolar macrophages (AMs) in patients with idiopathic pulmonary fibrosis (IPF). METHODS: The PKC activity of AM in 9 healthy volunteers and 15 patients with IPF was investigated by measuring the radioactivity. RESULTS: The total, cytosolic and membrane PKC activity of AM in bronchoalveolar lavage fluid (BALF) from patients with IPF were higher than those from control group (P < 0.01, P < 0.05 and P < 0.05, respectively). The total and the membrane-associated PKC activity had a positive correlation with the number of cells in BALF (r = 0.8135, P < 0.01 and r = 0.5917, P < 0.05), respectively. CONCLUSION: As a bypass of transmembrane signal transduction, PKC was suggested to be involved in the origination and development of IPF.

Adult↗
PubMed1993

Idiopathic pulmonary fibrosis and hepatitis C virus infection.

A possible role for hepatitis C virus (HCV) infection in the pathogenesis of idiopathic pulmonary fibrosis (IPF) has recently been suggested on the basis of an unusually high seroprevalence rate of anti-HCV in such patients from Japan. In an attempt to confirm these findings, we tested sera from 62 patients with IPF by two second-generation anti-HCV ELISAs. Only one serum was reactive. Serum from this patient gave an indeterminate result when tested by four-antigen RIBA (c22 band only), and it was negative for the presence of HCV RNA when tested by the reverse transcriptase polymerase chain reaction assay. HCV infection is thus no more prevalent in patients with IPF from the UK than in the general population.

Aged↗
PubMed2000

[Clinical significance of pattern types in high resolution computed tomography images of patients with idiopathic pulmonary fibrosis].

UNLABELLED: The aim of the study was to assess significance of two types of HRCT pattern in patients with idiopathic pulmonary fibrosis (IPF), corresponding to usual interstitial pneumonia. The study population consisted of 34 patients, 11 women and 23 men, mean age 64.5 +/- 10.5 years. The patients were divided into two groups according to HRCT appearance: Group A--reticular pattern with some ground-glass attenuation (30 patients); group B--reticular pattern only (4 patients). Age, level of dyspnea, pulmonary function tests were similar in both groups. Longer history of dyspnea and more frequent finger clubbing (all patients) were found in Group B. 30 patients were followed-up for at least 12 months. In this period 4 out of 27 patients died in Group A, and 2 out of 3 patients died in Group B (p < 0.05). CONCLUSION: HRCT showing reticular pattern only corresponds to late phase of IPF and is connected with very short survival.

Aged↗
PubMed1995

Superoxide anion formation and glutathione metabolism of blood in patients with idiopathic pulmonary fibrosis.

The oxidant-antioxidant imbalance in the lower respiratory tract plays a major role in the pathogenesis in idiopathic pulmonary fibrosis (IPF). However, the systemic oxidant-antioxidant balance in the patients with IPF has not been extensively evaluated. In this study, the metabolism of glutathione (GSH) and superoxide anion production of whole blood were tested in 14 IPF patients and 12 normal subjects. While the total amount of GSH in the blood of IPF patients was not different from that of normal subjects (IPF; 22.9 +/- 4.9 micrograms/ml, control; 26.1 +/- 3.7 micrograms/ml), the amount of oxidized GSH (GSSG) and the ratio of GSSG to the total GSH in blood significantly increased in patients with IPF (IPF; 14.4 +/- 3.5%, control; 7.0 +/- 1.7%, P < 0.01), indicating that the glutathione redox cycle may be impaired in IPF. The production and generation of superoxide anions by blood were significantly greater in IPF than in normal subjects. The level of superoxide anion production was correlated with the GSSG/GSH ratio. These results indicate that IPF patients exhibit an impaired GSH metabolism with an increased oxidant formation of blood.

Adult↗
PubMed1995

Relationship between cells obtained by bronchoalveolar lavage and survival in idiopathic pulmonary fibrosis.

BACKGROUND: The relationship between cell types in bronchoalveolar lavage (BAL) fluid and the clinical course of patients with idiopathic pulmonary fibrosis (IPF) has been the subject of several studies. However, the results of these studies are not conclusive. The aim of this study was to investigate the relationship between the absolute and relative cell numbers in BAL fluid from patients with IPF and their survival. METHODS: Results obtained from the initial BAL fluid analyses of all histologically proven cases of IPF (n = 49) were selected retrospectively. Cox's proportional hazards survival analysis was used for estimating the relationship between absolute and relative cell numbers and survival. RESULTS: A negative relationship was found between both the absolute numbers and percentages of eosinophils in BAL fluid samples and survival. No such relationship was demonstrated for the absolute numbers or the percentages of any other cell type. CONCLUSIONS: Although this study has restrictions, these findings suggest a negative relationship between the absolute numbers and percentages of eosinophils in BAL fluid samples and survival in patients with IPF.

Adult↗
PubMed1977

Analysis of cellular and protein content of broncho-alveolar lavage fluid from patients with idiopathic pulmonary fibrosis and chronic hypersensitivity pneumonitis.

To evaluate cellular and protein components in the lower respiratory tract of patients with idiopathic pulmonary fibrosis (IPF) and chronic hypersensitivity pneumonitis (CHP), limited broncho-alveolar lavage was done in 58 patients (19 IPF, 7 CHP, and 32 controls). Analysis of the cells and protein in the lavage fluids from patients with IPF revealed an inflammatory and eosinophilic response and a significant elevation of IgG in the lungs. With corticosteroid therapy, inflammation diminished but eosinophils remained. Lavage fluid from patients with CHP also had eosinophils and elevated levels of IgG. However, in contrast to IPF, lavage fluid from CHP patients contained IgM, fewer inflammatory cells, and a strikingly increased number (38-74%) of lymphocytes. Identification of lavage lymphocytes in CHP showed that T lymphocytes were significantly elevated and B lymphocytes were decreased compared to peripheral blood. These studies suggest nthat the lung in IPF and CHP may function as a relatively independent immune organ, and that analysis of cells and proteins in broncho-alveolar lavage fluid may be of diagnostic, therapeutic, and investigative value in evaluating patients with fibrotic lung disease.

Aged↗