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PubMed2002

Bleomycin hydrolase and a genetic locus within the MHC affect risk for pulmonary fibrosis in mice.

Susceptibility to pulmonary fibrosis following environmental insults or cytotoxic cancer therapies has a genetic component. In mouse strains differing in susceptibility to bleomycin-induced lung fibrosis, we show highly significant linkage to only two loci. The first locus on chromosome 17 in the major histocompatibility complex (MHC), LOD = 17.4, named Blmpf1, is highly significant in both males and females, and accounts for approximately 20% of the phenotypic variance. We confirmed the presence of Blmpf1 in MHC congenic mice and narrowed the region to 2.7 cM in a reduced MHC congenic strain. The second locus on chromosome 11, LOD = 5.6, named Blmpf2, is significant in males only. A model including an interaction between Blmpf1 and Blmpf2 best fit the data in males. We confirmed Blmpf2 in a chromosome substitution strain, C57BL/6J-11(C3H), and found that its presence reduces the severity of fibrosis. Functional studies of bleomycin hydrolase activity indicate that this enzyme modulates bleomycin-induced pulmonary fibrosis, suggesting that it may be a candidate gene for Blmpf2. The data suggest sex-specific models of susceptibility to bleomycin-induced lung fibrosis, with an interaction between Blmpf2 and Blmpf1 for the more susceptible males and Blmpf1 as the major locus in females. A putative mechanism for the interaction between the two loci in males is that bleomycin hydrolase functions as an MHC class I epitope-processing protease.

Animals↗

PubMed2005

Sputum eosinophilia in idiopathic pulmonary fibrosis.

OBJECTIVES AND DESIGN: Cough is a common symptom in idiopathic pulmonary fibrosis that is difficult to treat and has a major impact on quality of life. We tested the hypothesis that the cough and increased cough reflex sensitivity seen in patients with idiopathic pulmonary fibrosis may be due to airway inflammation in a prospective, cross-sectional study. SUBJECTS AND METHODS: We measured the induced sputum inflammatory cell profile and cell-free supernatant inflammatory mediator concentrations in 15 patients with idiopathic pulmonary fibrosis, 17 healthy controls and 15 patients with chronic obstructive pulmonary disease. RESULTS: Both the geometric mean sputum differential eosinophil cell count and median eosinophilic-cationic-protein concentration were significantly higher in patients with idiopathic pulmonary fibrosis than controls (2.1% vs 0.3%; p <0.001 and 1.1 mg/ml versus 0.2 mg/ml; p=0.03 respectively). There were no significant differences in sputum eosinophil counts and eosinophilic-cationic-protein concentrations between patients with idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease. Sputum leukotriene-B4 concentrations were significantly lower in patients with idiopathic pulmonary fibrosis (p=0.03) and chronic obstructive pulmonary disease (p=0.008) compared to controls. CONCLUSIONS: Idiopathic pulmonary fibrosis is characterised by the presence of active eosinophilic airway inflammation raising the possibility that airway inflammation may contribute to symptoms such as cough.

Aged↗

PubMed2006

Immunomodulation of experimental pulmonary fibrosis by intravenous immunoglobulin (IVIG).

OBJECTIVES: To assess the immunomodulatory effect of intravenous immunoglobulin (IVIG) using an experimental model of bleomycin-induced pulmonary fibrosis. METHODS: Pulmonary fibrosis was induced in C57BL/6 mice by direct intratracheal injection of bleomycin. Mice were treated with IVIG 1 week prior to (prevention protocol), or 10 days following bleomycin injection, when the disease was in progress. The controls used in the study included mice given phosphate buffered saline (PBS) and mice subjected to a commercial individual-IgG. Collagen-I deposits in the affected lungs were detected by Sirius red staining of paraffin embedded lung sections. The collagen-I content was measured by employing the hydroxyproline assay. RESULTS: Prevention of bleomycin-induced pulmonary fibrosis by IVIG has been demonstrated by reduced expression of collagen-I protein in the affected lungs. The hydroxyproline levels in the lungs of the IVIG-treated mice were 214.33 +/- 13.56 microg/1 g tissue, compared to the higher levels in lungs of IgG treated mice (342.44 +/- 35.60 microg/1 g tissue) or untreated controls 328.00 +/- 45.55 microg/1 g tissue, (p < 0.0001). Effective treatment of bleomycin-induced pulmonary fibrosis by IVIG has been demonstrated by the reduced expression of collagen-I protein in the affected lungs, detected by sirius red histological staining. The hydroxyproline levels in the lungs of the IVIG-treated mice were 261.00 +/- 18.81 microg/1 g tissue, in comparison to the higher levels in the lungs of the IgG treated mice (342.43 +/- 32.89 microg/1 g tissue) and of untreated controls (344.33 +/- 49.85 microg/1 g tissue), (p < 0.001). CONCLUSIONS: Based on these preliminary studies, we conclude that IVIG may have a beneficial effect in the down regulation of collagen-I levels in the lungs of mice with bleomycin-induced pulmonary fibrosis.

Animals↗

PubMed1978

Gallium-67 citrate scanning in the staging of idiopathic pulmonary fibrosis: Correlation and physiologic and morphologic features and bronchoalveolar lavage.

Idiopathic pulmonary fibrosis is a fatal disorder characterized by interstitial fibrosis and parenchymal inflammation. Current concepts of this disease suggest that the inflammation precedes and probably induces the fibrotic state. To evaluate the extent and relative activity of the inflammatory process, we scanned patients with idiopathic pulmonary fibrosis using gallium-67, a radionuclide known to concentrate in regions of inflammation. To quantify the amount of isotope in the lung parenchyma, the 67Ga-index was developed, a parameter derived from estimates of the size of regional pulmonary uptake, the uptake intensity, and its texture. Evaluation of 67Ga scans in 30 patients with idiopathic pulmonary fibrosis and 19 control subjects demonstrated that the 67Ga-index in the group with idiopathic pulmonary fibrosis was significantly higher (P less than 0.001) than that in the control group. When compared with lung biopsy morphologic studies in 22 patients with idiopathic pulmonary fibrosis, the 67Ga-index correlated with the degree of interstitial cellularity (P less than 0.05) and the degree of alveolar cellularity (P less than 0.005). When compared with cellular analysis of bronchoalveolar lavage fluid in 17 patients with idiopathic pulmonary fibrosis, the 67Ga-index correlated with the differential percentage of neutrophils (P less than 0.05), but not lymphocytes, eosinophils, or macrophages. These studies indicate that 67Ga accumulates in the lungs of patients with idiopathic pulmonary fibrosis and is probably associated with the active inflammatory state. The associations of the 67Ga-index with morphologic features and bronchoalveolar lavage analysis suggest that quantitative evaluation of these scans may be useful in staging the activity of idiopathic pulmonary fibrosis and following responses to therapy.

Adult↗

PubMed2006

The genetic approach in pulmonary fibrosis: can it provide clues to this complex disease?

Multiple investigators have undertaken genetic studies in idiopathic pulmonary fibrosis populations in attempts to define genetic links to disease in hopes that this would improve understanding of disease pathogenesis and target pathways for therapy. Multiple genes have been evaluated using a candidate gene approach with limited success, with results suggesting a disease modifier effect rather than a disease causing effect. Using this approach, associations have been observed between idiopathic pulmonary fibrosis and specific polymorphisms in genes encoding interleukin-1 receptor antagonist, tumor necrosis factor-alpha, and complement receptor 1. Recently investigators have used familial pulmonary fibrosis cohorts to evaluate for genetic mutations associated with idiopathic pulmonary fibrosis. Using one pulmonary fibrosis kindred, a mutation in the gene encoding surfactant protein C was identified as the cause of pulmonary fibrosis in this family. Subsequently, another individual with idiopathic pulmonary fibrosis was identified with a different mutation in surfactant protein C. Though rarely found in patients with idiopathic pulmonary fibrosis, these surfactant protein C mutations highlight the importance of the alveolar epithelium in disease pathogenesis. A recent collaboration between investigators at three major centers has resulted in the largest collection of families with pulmonary fibrosis to date, with hopes that this effort will identify genetic mutations associated with idiopathic pulmonary fibrosis. If genetic links to idiopathic pulmonary fibrosis are defined in this study, then the pathways involved with these genes and gene products can be targeted by investigators to help identify potential treatment options for this disease.

Cytokines↗

PubMed1983

Amiodarone and pulmonary fibrosis.

Of 25 cases of idiopathic pulmonary fibrosis, confirmed by open chest lung biopsy between January 1979 and July 1981, 5 patients had been taking amiodarone in doses less than 600 mg daily for 1 to 6 years. No lung disease had been observed in any patient before the administration of amiodarone, and other drugs, factors and diseases thought to play a role in the causation of pulmonary fibrosis were ruled out. Two patients died of respiratory insufficiency, and only 1 does not now suffer from serious sequelae. Review of a further 5 cases reported in the literature and the present data suggest a causal link between administration of amiodarone and pulmonary fibrosis, and tend to indicate a hypersensitivity mechanism.

Aged↗

PubMed2005

[Successful treatment of a severe case of idiopathic pulmonary fibrosis with rapamycin].

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive chronic disorder of the lower respiratory tract. The main clinical feature is a progressive shortness of breath, particularly on exercise. An overproduction and deposition of collagen and a proliferation of mesenchymal cells are the histopathologic characteristics. Rapamycin is an immunosuppressive agent with antiproliferative effects on mesenchymal cells including fibroblasts. It was this rationale that prompted the authors to administer rapamycin in a case of rapidly progressive IPF. CASE REPORT: In a 73-year-old female with a 2-month history of IPF, treatment with steroids and interferon gamma-1b did not improve the detrimental clinical course. Treatment with rapamycin was started; subsequently, clinical condition and objective findings improved markedly within weeks. She is now under treatment for 18 months. CONCLUSION: The authors presume that partial remission is related to rapamycin which may be effective in blocking the progressive fibrosis and increased collagen synthesis thought to be pathophysiologically relevant in this disease. Further studies have to show whether rapamycin may be a treatment option in idiopathic pulmonary fibrosis.

Aged↗

PubMed2004

Bone marrow-derived progenitor cells in pulmonary fibrosis.

The origin of fibroblasts in pulmonary fibrosis is assumed to be intrapulmonary, but their extrapulmonary origin and especially derivation from bone marrow (BM) progenitor cells has not been ruled out. To examine this possibility directly, adult mice were durably engrafted with BM isolated from transgenic mice expressing enhanced GFP. Induction of pulmonary fibrosis in such chimera mice by endotracheal bleomycin (BLM) injection caused large numbers of GFP(+) cells to appear in active fibrotic lesions, while only a few GFP(+) cells could be identified in control lungs. Flow-cytometric analysis of lung cells confirmed the BLM-induced increase in GFP(+) cells in chimera mice and revealed a significant increase in GFP(+) cells that also express type I collagen. GFP(+) lung fibroblasts isolated from chimera mice expressed collagen and telomerase reverse transcriptase but not alpha-smooth muscle actin. Treatment of isolated GFP(+) fibroblasts with TGF-beta failed to induce myofibroblast differentiation. Cultured lung fibroblasts expressed the chemokine receptors CXCR4 and CCR7 and responded chemotactically to their cognate ligands, stromal cell-derived factor-1 alpha and secondary lymphoid chemokine, respectively. Thus the collagen-producing lung fibroblasts in pulmonary fibrosis can also be derived from BM progenitor cells.

Actins↗

PubMed2004

Increased level of soluble E-selectin in the serum from patients with idiopathic pulmonary fibrosis.

To elucidate the biological significance of selectin for idiopathic pulmonary fibrosis, we titrated the serum soluble E-selectin. From 31 cases of idiopathic pulmonary fibrosis patients without signs or symptoms of infection, the serum was obtained and the concentration was titrated by enzyme-linked immunosorbent assay. The serum soluble E-selectin titer was significantly higher than that of healthy controls. However, significant elevation was not observed in the sera from the patients with other pulmonary diseases, such as pulmonary emphysema, sarcoidosis, or bronchiectasis. In the patients with idiopathic pulmonary fibrosis, the number of white blood cells, C-reactive protein or lactate dehydrogenase activity did not show a significant relationship with the soluble E-selectin titer. About 16 out of the 31 idiopathic fibrosis patients, the serum surfactant apoprotein-A titer, which is a parameter of the disease activity of idiopathic pulmonary fibrosis, was also tested. The surfactant apoprotein-A titer was loosely correlated with the soluble E-selectin titer. These observations suggest that E-selectin may be relevant to the pathogenesis of idiopathic pulmonary fibrosis, and it may be a novel clinical parameter for idiopathic pulmonary fibrosis.

Adult↗

PubMedDate not supplied

Is "tumor necrosis factor" the major effector of pulmonary fibrosis?

A major role of TNF in pulmonary fibrosis is supported by the following evidences obtained from pulmonary fibrosis induced in mice by bleomycin or silica particles; 1) these diseases are associated with a marked and lasting increase of the TNF mRNA within the lung, 2) they can be prevented by a treatment with anti TNF antibody or aggravated by a perfusion of mouse recombinant TNF, 3) an infusion of TNF-alpha can reproduce the alterations observed during pulmonary fibrosis such as growth of fibroblasts, collagen deposition, cell necrosis.

Animals↗

PubMed1988

Apical pulmonary fibrosis in psoriasis.

Apical pulmonary fibrosis has been established as a non-articular complication of ankylosing spondylitis. Although psoriasis is frequently associated with arthropathy and spondylitis, there is only one previous report of apical fibrosis occurring in a patient with psoriasis. We report two patients with psoriasis complicated by apical pulmonary disease in whom extensive investigations were negative.

Aged↗

PubMed2004

Diagnostic relevance of Langerin detection in cells from bronchoalveolar lavage of patients with pulmonary Langerhans cell histiocytosis, sarcoidosis and idiopathic pulmonary fibrosis.

The diagnosis of pulmonary Langerhans cell histiocytosis might be refined by demonstrating reliability of a new cell marker, i.e., Langerin (CD207), used on bronchoalveolar lavage fluid. For this purpose, we collected material from patients with this disease and also with sarcoidosis and idiopathic pulmonary fibrosis as controls. In addition to the immunocytochemical detection of Langerin, we examined the expression profiles of CD1a and the macrophage tandem-repeat mannose receptor (CD206). To test accessibility of Langerin, a C-type lectin, for mannosides, we employed reverse lectin histochemistry using mannose-containing neoglycoproteins. The analysis revealed a significantly increased percentage of CD1a- and Langerin-positive cells in pulmonary Langerhans cell histiocytosis in comparison with both other studied diseases. No expression of the 175-kDa mannose-binding lectin (CD206) in Langerhans cells was observed. Evidently, binding sites on the cells were not accessible for the mannose-containing neoglycoligand. These results provide evidence for the usefulness of Langerin-directed immuno- and glycohistochemical monitoring of bronchoalveolar lavage fluid in the diagnosis of pulmonary Langerhans cell histiocytosis.

Adult↗

PubMedDate not supplied

Pulmonary fibrosis induced by cyclophosphamide.

OBJECTIVE: To report a case of pulmonary fibrosis resulting from use of cyclophosphamide as chemotherapy to treat a patient with breast cancer. CASE SUMMARY: We describe the case of a 52-year-old woman with breast cancer who developed pulmonary fibrosis after four cycles of chemotherapy that included cyclophosphamide. Pulmonary function tests revealed the presence of a severe ventilatory restriction. The open lung biopsy revealed pulmonary fibrosis with vascular sclerosis and signs of pulmonary hypertension. DISCUSSION: Cyclophosphamide is an alkylating agent that has been associated with interstitial pneumonia and pulmonary fibrosis. The frequency of these unwanted effects is <1%. The clinical picture consists of the progressive appearance of dyspnea and a non-productive cough that progresses to severe pulmonary insufficiency. The risk factors described for these complications have been the use of chemotherapy regimens that include other drugs with known pulmonary toxicities, the cumulative total dose, the addition of radiotherapy, and the use of high doses of cyclophosphamide. CONCLUSIONS: Even though the frequency of pulmonary fibrosis in patients treated with cyclophosphamide-based chemotherapy regimens is low, the presence of dyspnea and an interstitial pattern in a patient makes it necessary to consider that possible drug toxicity. The open lung biopsy is the most accurate diagnostic technique for these cases. The discontinuation of cyclophosphamide and treatment with corticosteroids is usually followed by clinical recovery in approximately 50% of patients and, in some cases, reversal of the lung injury.

Antineoplastic Agents, Alkylating↗

PubMed1999

A preliminary study of long-term treatment with interferon gamma-1b and low-dose prednisolone in patients with idiopathic pulmonary fibrosis.

BACKGROUND AND METHODS: Patients with idiopathic pulmonary fibrosis have progressive scarring of the lung and usually die within four to five years after symptoms develop. Treatment with oral glucocorticoids is often ineffective. We conducted an open, randomized trial of treatment with a combination of interferon gamma-1b, which has antifibrotic properties, and an oral glucocorticoid. We studied 18 patients with idiopathic pulmonary fibrosis who had not had responses to glucocorticoids or other immunosuppressive agents. Nine patients were treated for 12 months with oral prednisolone alone (7.5 mg daily, which could be increased to 25 to 50 mg daily), and nine with a combination of 200 microg of interferon gamma-1b (given three times per week subcutaneously) and 7.5 mg of prednisolone (given once a day). RESULTS: All the patients completed the study. Lung function deteriorated in all nine patients in the group given prednisolone alone: total lung capacity decreased from a mean (+/-SD) of 66+/-8 percent of the predicted value at base line to 62+/-6 percent at 12 months. In contrast, in the group receiving interferon gamma-1b plus prednisolone, total lung capacity increased (from 70+/-6 percent of the predicted value at base line to 79+/-12 percent at 12 months, P<0.001 for the difference between the groups). In the group that received interferon gamma-1b plus prednisolone, the partial pressure of arterial oxygen at rest increased from 65+/-9 mm Hg at base line to 76+/-8 mm Hg at 12 months, whereas in the group that received prednisolone alone it decreased from 65+/-6 to 62+/-4 mm Hg (P<0.001 for the difference in the change from baseline values between the two groups); on maximal exertion, the value increased from 55+/-6 to 65+/-8 mm Hg in the group that received combined treatment and decreased from 55+/-6 mm Hg to 52+/-5 mm Hg in the group given prednisolone alone (P<0.001). The side effects of interferon gamma-1b, such as fever, chills, and muscle pain, subsided within the first 9 to 12 weeks. CONCLUSIONS: In a preliminary study, 12 months of treatment with interferon gamma-1b plus prednisolone was associated with substantial improvements in the condition of patients with idiopathic pulmonary fibrosis who had had no response to glucocorticoids.

Carrier Proteins↗

PubMed1998

Amiodarone induced pulmonary fibrosis in infancy.

We report a case of pulmonary fibrosis in an infant receiving amiodarone for treatment of intractable atrioventricular reentrant tachycardia secondary to Wolff-Parkinson-White syndrome. At 9 months, a screening chest radiograph showed a diffuse interstitial infiltrate in an asymptomatic, thriving infant. Amiodarone was discontinued and the pulmonary fibrosis resolved gradually over 6 months. This case documents the first report of amiodarone induced pulmonary fibrosis in the pediatric age group. We speculate that as amiodarone is used more frequently to manage pediatric arrhythmias, pulmonary fibrosis, a known complication of this antiarrhythmia in adults may be seen with increasing frequency in children.

Adrenergic beta-Antagonists↗

PubMed1993

[Cell-associated interleukin 1 production of alveolar macrophages from bleomycin-induced pulmonary fibrosis in rats].

In order to clarify the mechanisms of pulmonary fibrosis, we produced bleomycin (BLM)-induced pulmonary fibrosis in rats and examined the ability of alveolar macrophages (AM) to produce interleukin-1 (IL-1). BLM (0.9 mg) was administered once via the trachea to male Wistar rats weighing about 200 g. Bronchoalveolar lavage was performed at 1, 3, 6, 9 and 12 days after administration. AM were incubated for 24 hours, then extracellular IL-1 in the supernatants and cell-associated IL-1 of AM were measured by proliferation assay of mouse thymocytes. Cell-associated IL-1 activity was measured after fixation by paraformaldehyde (PFA). Extracellular IL-1 was detected in the culture media of AM at only day 1 after administration. On the other hand, cell-associated IL-1 was detected in AM fixed by PFA on days 1, 3, 6 and 9 after administration. AM from BLM-induced pulmonary fibrosis in rats were fixed by PFA and then were treated with anti-IL-1 alpha antibody or anti-IL-1 beta antibody. Cell-associated IL-1 activity was neutralized by treatment with anti-IL-1 alpha antibody and was not neutralized by treatment with anti-IL-1 beta antibody. Following this, the effect of cell-associated IL-1 on pulmonary fibroblasts was examined. This was estimated by the proliferation of pulmonary fibroblasts using incorporation of 3H-thymidine. When pulmonary fibroblasts were incubated with AM fixed by PFA from BLM-induced pulmonary fibrosis in rats, proliferation of pulmonary fibroblasts was inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effects of the 21-aminosteroid, U74389F, on bleomycin-induced pulmonary fibrosis in rats.

OBJECTIVE: To determine if a new class of agents, the 21-aminosteroids, which are reportedly potent inhibitors of iron-dependent lipid peroxidation, could protect rats from bleomycin-induced pulmonary fibrosis. SUBJECTS: Fifty-five adult male Sprague-Dawley rats. DESIGN: Prospective, randomized, blinded, controlled trial. INTERVENTIONS: The rats were subjected to intratracheal bleomycin (or saline vehicle), and were then treated with the 21-aminosteroid, U74389F (20 mg/kg/day), or vehicle, for the next 7 days. MEASUREMENTS AND MAIN RESULTS: At 21 days after bleomycin administration, pulmonary fibrosis was assessed histologically as percent of lung fields with evidence of fibrosis. Pulmonary fibrosis was assessed biochemically by measuring pulmonary elastin and hydroxyproline content. To determine if a protective effect of U74389F was linked to the 21-aminosteroid's ability to suppress lipid peroxidation, two products of lipid peroxidation were assayed in the lungs at 7 and 14 days after bleomycin exposure. By histologic assessment, the 21-aminosteroid-treated, bleomycin-exposed animals were found to have significantly decreased the extent of pulmonary fibrosis when compared with the bleomycin control group (mean 48.6 +/- 20.0 [SD] % [n = 9] vs. 68.4 +/- 19.6% [n = 11]; p < .05). In addition, lung elastin was decreased by approximately 75% (p < .05) and hydroxyproline was decreased by approximately 50% (NS) in the 21-aminosteroid-treated group when compared with the bleomycin control group. At 7 and 14 days after bleomycin exposure, all bleomycin-exposed animals had evidence of increased lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances), but the 21-aminosteroid-treated, bleomycin-exposed animals had significantly decreased evidence of lipid peroxidation when compared with bleomycin controls. CONCLUSIONS: The 21-aminosteroid can substantially protect animals from bleomycin-induced pulmonary fibrosis and may prove useful in other lung diseases where iron-dependent, free-radical reactions and/or lipid peroxidation are presumed mechanisms of toxicity.

Animals↗

PubMed2001

Protection from pulmonary fibrosis in the absence of CCR2 signaling.

Pulmonary fibrosis can be modeled in animals by intratracheal instillation of FITC, which results in acute lung injury, inflammation, and extracellular matrix deposition. We have previously shown that despite chronic inflammation, this model of pulmonary fibrosis is lymphocyte independent. The CC chemokine monocyte-chemoattractant protein-1 is induced following FITC deposition. Therefore, we have investigated the contribution of the main monocyte-chemoattractant protein-1 chemokine receptor, CCR2, to the fibrotic disease process. We demonstrate that CCR2(-/-) mice are protected from fibrosis in both the FITC and bleomycin pulmonary fibrosis models. The protection is specific for the absence of CCR2, as CCR5(-/-) mice are not protected. The protection is not explained by differences in acute lung injury, or the magnitude or composition of inflammatory cells. FITC-treated CCR2(-/-) mice display differential patterns of cellular activation as evidenced by the altered production of cytokines and growth factors following FITC inoculation compared with wild-type controls. CCR2(-/-) mice have increased levels of GM-CSF and reduced levels of TNF-alpha compared with FITC-treated CCR2(+/+) mice. Thus, CCR2 signaling promotes a profibrotic cytokine cascade following FITC administration.

Animals↗