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PubMed2005

Nodular scleroderma: increased expression of connective tissue growth factor.

BACKGROUND: Nodular scleroderma is a fibrosing reaction, presenting well-defined, firm, raised nodules, which resembles keloid. Recent studies suggest that connective tissue growth factor (CTGF) is involved in the fibrotic process, and its expression is increased in many fibrosing diseases. OBJECTIVE: In this study, we report 3 cases of nodular scleroderma, and the expression of CTGF is also investigated. METHODS: Three patients who developed nodular scleroderma are described. Expression of CTGF protein and transcripts in nodular scleroderma was examined by immunohistochemistry and in situ hybridization. RESULTS: Patients were 1 female and 2 males, and all cases were associated with diffuse systemic sclerosis. Nodular lesions were found on the chest (2 cases), back (1 case), upper arm (1 case) and nape (1 case). Histology of the nodular lesions showed thickened collagen bundles in the dermis. Results of immunohistochemistry showed that expression of CTGF was detected on the sclerotic fibroblasts in the lesions of nodular scleroderma, while it was not detected in fibroblasts in normal skin. In situ expression of CTGF transcripts was abundantly detected on the fibroblastic cells in nodular scleroderma. CONCLUSION: Our data showed increased expression of CTGF in the sclerotic fibroblasts of nodular scleroderma, suggesting that CTGF plays an important role in its pathogenesis.

Adult↗
PubMed1995

The challenge of chagasic cardiomyopathy. The pathologic roles of autonomic abnormalities, autoimmune mechanisms and microvascular changes, and therapeutic implications.

The evidence provided by both human and animal studies on chronic Chagas' heart disease suggests that the cardiomyopathy occurs as a consequence of several physiopathological processes occurring after infection interacting with unidentified host factors. The development of the chronic fibrosing myocarditis is related to progressive and additive focal cellular necrosis, and associated inflammatory lymphomononuclear infiltrate and reactive and reparative myocardial fibrosis and surrounding myocyte hypertrophy. These processes may be initiated and perpetuated by alterations in the myocardial microcirculation and by autoimmune factors. The autonomic impairment and/or the chronic fibrosing myocarditis and the left ventricular dysfunction could act as factors predisposing one to an increased risk of sudden cardiac death.

Animals↗
PubMed1989

Quantitative estimation of the collagen content in normal and pathologic pancreas tissue.

The aims of the study were to measure the collagen content in pancreas using a colorimetric method and to compare the amount of collagen in normal pancreas (11 cases), diffuse fibrosing pancreatitis (17 cases), and chronic calcifying pancreatitis (11 cases). The procedure of fibrosis measurement was based on the selective capacity of two dyes, Sirius red and fast green, to set on collagen and noncollagenous proteins, respectively. After staining of sections, colors were eluted from the sections and the specific absorbance of each eluted dye was read on a spectrophotometer. The collagen content in normal pancreata was 26.5 +/- 7.2 micrograms collagen/mg protein. The amount of collagen increased with the age of patients: the mean value of the patients under the age of 50 was 18.2 +/- 4 micrograms collagen/mg protein whereas the mean value in older patients was 31.9 +/- 8 micrograms collagen/mg protein (p less than 0.01). The value of collagen in pancreas with a diffuse fibrosing pancreatitis was 44.7 +/- 7.5 micrograms collagen/mg protein. This value was significantly different from the collagen content in normal pancreas (p less than 0.001) and in pancreas with a chronic calcifying pancreatitis (77.9 +/- 8 micrograms collagen/mg protein, p less than 0.001). This method permits discrimination between different chronic diseases that can also be differentiated on a histopathologic basis.

Adult↗
PubMed1995

Clara cell protein (CC-16) induces a phospholipase A2-mediated inhibition of fibroblast migration in vitro.

Clara cell protein (CC-16, also designated CC-10) is synthesized by the bronchiolar epithelium and has been suggested as an inhibitor of phospholipase A2 (PLA2) activity. Therefore, CC-16 is a candidate for controlling inflammatory events in the lung. Because CC-16 amounts and function may be altered in fibrosing lung diseases in which bronchiolar injury has been reported, it was measured in alveolar fluids and sera. Secretory PLA2 activity in alveolar fluids and the influence of CC-16 on platelet-derived growth factor-induced human fibroblast chemotaxis and cytosolic PLA2 activity were also explored. CC-16 content was decreased in alveolar fluids from idiopathic pulmonary fibrosis (IPF: 1.3 +/- 0.1 mg/L) and bleomycin lung (1.1 +/- 0.2 versus 2.1 +/- 0.2 mg/L in controls, p < 0.05), whereas there was a three- to ninefold increase in secretory PLA2 activity (p < 0.05 versus controls). CC-16 inhibited fibroblast chemotaxis in a dose-dependent manner (90% inhibition at 30 micrograms/ml CC-16). This inhibition was reversed by reducing CC-16. CC-16 was also able to lower fibroblastic cytosolic PLA2 activity by 50% in vitro. In summary, CC-16 is able to inhibit fibroblast chemotaxis in vitro by mechanisms that may be related to a blockage of cytosolic PLA2 activity. It can be postulated that CC-16 deficiency may contribute to fibroblast burden activity in fibrosing lung diseases.

Adult↗
PubMed1998

8-Isoprostane as a biomarker of oxidative stress in interstitial lung diseases.

Oxidative stress contributes to the pathophysiology of interstitial lung diseases, such as cryptogenic fibrosing alveolitis (CFA), fibrosing alveolitis associated with systemic sclerosis (FASSc) and sarcoidosis. F2-isoprostanes are a series of prostaglandin (PG) F2-like compounds produced in vivo independent of cyclooxygenase, as products of the radical-catalyzed lipid peroxidation. Measurement of the concentrations of F2-isoprostanes has proved to be valuable in assessing oxidative stress in vivo. The aim of this study was to measure 8-epi-PGF2alpha concentrations, one of the most abundant F2-isoprostane in humans, in bronchoalveolar lavage (BAL) in normal subjects and to compare them to those observed in patients with CFA (n = 9), FASSc (n = 8) and sarcoidosis (n = 10). 8-epi-PGF2alpha was detectable in BAL fluid in normal subjects (9.6 +/- 0.8 pg/ml) and its concentrations were increased approximately 5-fold in patients with CFA (47.4 +/- 7.0, p < 0.001) and FASSc (43.2 +/- 3.3, p < 0. 001). 8-epi-PGF2alpha was also increased in patients with sarcoidosis, although to a lesser extent (12.0 +/- 0.70 pg/ml, p < 0. 01). No correlation between 8-epi-PGF2alpha and either lung function tests or BAL cell types was observed in any group of patients. Our study shows that the level of oxidative stress is enhanced in patients with interstitial lung diseases as reflected by increased concentrations of 8-epi-PGF2alpha in BAL fluid.

Adult↗
PubMed1988

Cadmium-chloride-induced air-space enlargement with interstitial pulmonary fibrosis is not associated with destruction of lung elastin. Implications for the pathogenesis of human emphysema.

To determine whether lung elastin is lost during the evolution of cadmium-induced air-space enlargement with pulmonary fibrosis, the lung elastin of 5- to 7-day-old golden Syrian hamster pups was radiolabeled by giving [3H]valine. At maturity, a single intratracheal instillation of 0.5 ml of 0.025% CdCl2 solution was given. Lung mechanics, histologic examination, and biochemistry were studied 5, 10, 21, 42, 105, and 180 days after the cadmium treatment. The animals developed fibrosis and air-space enlargement with decreased lung volumes, compliance, and forced expiratory flow; their functional residual capacity was increased. The total lung collagen and total lung elastin were increased, but there was no loss of radiolabel in lung elastin. We conclude that CdCl2-induced air-space enlargement with pulmonary fibrosis is not accompanied by loss of neonatally formed lung elastic fibers. We hypothesize that air-space enlargement with fibrosis represents a stereotyped response of the lung to fibrosing injuries, which we hypothesize is due to forces from more fibrotic and atelectatic areas causing overdistension of less abnormal air spaces. The air-space enlargement of fibrosing human diseases such as sarcoidosis and eosinophilic granuloma may have a similar basis. Evidence is reviewed that human centrilobular emphysema may be a form of focal air-space enlargement with interstitial fibrosis; there may be mechanisms in addition to elastase-antielastase imbalance that cause human emphysema.

Animals↗
PubMed1999

Interferon-gamma upregulates the c-Met/hepatocyte growth factor receptor expression in alveolar epithelial cells.

In the repair process after lung injury, the regeneration of alveolar epithelial cells plays an important role by covering the damaged alveolar wall and preventing the activated fibroblasts from invading the intra- alveolar spaces. Hepatocyte growth factor (HGF) is a potent mitogen for alveolar epithelial cells and has been reported to be capable of repressing the fibrosing process by connecting to the c-Met/HGF receptor on alveolar epithelial cells. However, it has been reported that the c-Met expression was downregulated in an acute phase of lung injury, which may limit the effect of HGF for therapeutic use. In the present study we observed that interferon (IFN)-gamma upregulates the c-Met messenger RNA (mRNA) and protein expression in A549 alveolar epithelial cells. We analyzed the mechanism of this upregulation and found that IFN-gamma enhances the transcription of the c-met proto-oncogene, and that it does not prolong the stability of the c-Met mRNA. HGF is known to act as a motogen as well as a mitogen for epithelial cells. We also found that the migratory activity of A549 cells induced by HGF is strongly enhanced by preincubation with IFN-gamma. Finally, we administered recombinant IFN-gamma to C57BL/6 mice and confirmed that this upregulation is also observed in vivo. These results suggest that the combination of HGF and IFN-gamma could be a new therapeutic approach for fibrosing pulmonary diseases.

Animals↗
PubMed1988

Psychiatric consultations in rheumatology: a review of 100 cases.

Consultation-liaison psychiatry has contributed much to our understanding of the psychological complications of physical illness, both in general responses to illness and in particular problems related to specific diseases. We reviewed 100 psychiatric consultations from a specialized rheumatology unit. Eighty percent of the consultations consisted of patients with systemic lupus erythematosus (36%), rheumatoid arthritis (29%), and fibrositis (15%). The majority of S.L.E. patients had organic brain syndromes related to central nervous system involvement or corticosteroids, while the majority of rheumatoid arthritis patients had a depressive diagnosis. Fibrositis patients showed no specific psychiatric diagnosis. Some future areas of research for consultation-liaison psychiatry in this area are suggested.

Adaptation, Psychological↗
PubMed2006

IL18 and IL18R1 polymorphisms, lung CT and fibrosis: A longitudinal study in coal miners.

It has been suggested that interleukin (IL)-18 plays a role in the development of inflammatory and fibrosing lung diseases. Associations of polymorphisms in the genes coding for IL-18 (IL18 /G-656T, C-607A, G-137C, T113G, C127T) and its receptor (IL18R1 /C-69T) with coal workers' pneumoconiosis (CWP) were studied in 200 miners who were examined in 1990, 1994 and 1999. Coal-dust exposure was assessed according to job history and ambient measures. The main health outcome was lung computed tomography (CT) score in 1990. Internal coherence was assessed by studying CT score in 1994, 4-yr change in CT score and CWP incidence and prevalence. CT score in 1990 was a good predictor of radiographic grade in 1999 and, therefore, an appropriate subclinical quantitative trait. The IL18 -137C allele was associated with lower CT score in 1990 and 1994 (1.24 versus 1.69 and 1.57 versus 2.46, respectively), slower progression of CT score between 1990 and 1994 and lower pneumoconiosis prevalence in 1999 relative to the G allele (0.33 versus 0.77 and 8.2 versus 19.6%, respectively). Smoking- or dust-adjustment, and stratification on IL18R1 genotype and adjustment for haplotype effects did not change the conclusions. In conclusion, the results of the present study suggest a role for IL18 in reducing the development of this fibrosing lung disease.

Adult↗
PubMed1999

Clearance of inhaled technetium-99m-DTPA as a clinical index of pulmonary vascular disease in systemic sclerosis.

This study evaluated the utility of the clearance time of inhaled diethylenetriamine pentaacetate (DTPA) to distinguish pulmonary vascular disease from early fibrosing alveolitis (FA) in patients with systemic sclerosis (SSc). It was hypothesized that this would be preserved in patients with vascular disease compared with FA, despite similar gas-transfer deficits and matching lung volumes, because of the preservation of alveolar epithelial integrity. All patients had SSc and were categorized into a control group (C; n=9), pulmonary vascular group (VAS; n=14) or FA group (n=14) dependent on the appearance on a computed tomography (CT) scan and the transfer factor of the lung for carbon monoxide (T(L,CO)) (VAS and FA < or =70%, C > or =80%). All patients had a forced vital capacity (FVC) of >80%. The T(L,CO) (median) was similar in the VAS (57.5%) and FA (60%) groups. There was a significant difference in median DTPA clearance half-times between FA (21.25 min) and VAS (46.5 min) (p=0.014) and between FA and C (84.5 min) (p=0.0004). No difference was found between VAS and C (p=0.0778). Follow-up data from the VAS group showed no subsequent development of FA on the CT scan and no decrease in FVC (n=13, mean 42 months). These results suggest that clearance of diethylenetriamine pentaacetate is preserved in patients likely to have pulmonary vascular disease and may be useful in distinguishing fibrosing alveolitis from vascular disease in systemic sclerosis.

Adult↗
PubMed2000

Expression of growth factors, cytokines and matrix metalloproteinases in frozen shoulder.

Frozen shoulder is a chronic fibrosing condition of the capsule of the joint. The predominant cells involved are fibroblasts and myofibroblasts which lay down a dense matrix of type-I and type-III collagen within the capsule. This subsequently contracts leading to the typical features of pain and stiffness. Cytokines and growth factors regulate the growth and function of the fibroblasts of connective tissue and remodelling of the matrix is controlled by the matrix metalloproteinases (MMPs) and their inhibitors. Our aim was to determine whether there was an abnormal expression or secretion of cytokines, growth factors and MMPs in tissue samples from 14 patients with frozen shoulder using the reverse transcription/polymerase chain reaction (RT/PCR) technique and to compare the findings with those in tissue from four normal control shoulders and from five patients with Dupuytren's contracture. Tissue from frozen shoulders demonstrated the presence of mRNA for a large number of cytokines and growth factors although the frequency was only slightly higher than in the control tissue. The frequency for a positive signal for the proinflammatory cytokines Il-beta and TNF-alpha and TNF-beta, was not as great as in the Dupuytren's tissue. The presence of mRNA for fibrogenic growth factors was, however, more similar to that obtained in the control and Dupuytren's tissue. This correlated with the histological findings which in most specimens showed a dense fibrous tissue response with few cells other than mature fibroblasts and with very little evidence of any active inflammatory cell process. Positive expressions of the mRNA for the MMPs were also increased, together with their natural inhibitor TIMP. The notable exception compared with control and Dupuytren's tissue was the absence of MMP-14, which is known to be a membrane-type MMP required for the activation of MMP-2 (gelatinase A). Understanding the control mechanisms which play a part in the pathogenesis of frozen shoulder may lead to the development of new regimes of treatment for this common, protracted and painful chronic fibrosing condition.

Cytokines↗
PubMed2003

Terminal diffuse alveolar damage in relation to interstitial pneumonias. An autopsy study.

Acute exacerbations of idiopathic pulmonary fibrosis/cryptogenic fibrosing alveolitis (IPF/CFA) are rare and typically terminal events, but their relationship to underlying patterns of idiopathic interstitial pneumonias is unknown. We reviewed autopsy material from patients who died of diffuse alveolar damage in the clinical setting of pulmonary fibrosis, both idiopathic and with background fibrosing alveolitis with connective tissue disorders (FA-CTDs), and compared them with cases of acute interstitial pneumonia. Of 15 patients with acute exacerbations of IPF/CFA (n = 12) or FA-CTD (n = 3), 12 had a background pattern of usual interstitial pneumonia and 3 had fibrotic nonspecific interstitial pneumonia. All cases of fibrotic nonspecific interstitial pneumonia were seen in association with FA-CTD. The cause of acute exacerbations is unknown, but our data suggest that toxic effects of oxygen and triggering infection are unlikely causes. In patients with CTDs, it remains uncertain whether the acute exacerbation is related to the fibrosis, the associated CTD, or a combination of these factors. Acute exacerbations of IPF/CFA may be a more common terminal event than previously thought.

Aged↗
PubMed2004

Multifocal pleural cystic squamous metaplasia in a horse with chronic obstructive bronchopneumonia.

A 10-year-old Knabstrupper stallion was euthanatized because of severe dyspnea and exercise intolerance. Postmortem examination revealed diffuse severe alveolar emphysema and chronic fibrosing pleuritis of the caudal lung. Parts of both caudal lung lobes were covered with multiple raised firm gray to yellow plaques. Histologically, these areas consisted of circumscribed pleural fibroses and cysts of metaplastic keratinizing squamous epithelium. Immunohistochemistry revealed intense labeling for cytokeratins 5/6 and 10. In addition, caudal lung lobes were severely affected by a chronic partially obliterative bronchiolitis and peribronchiolitis with multifocal pleural involvement.

Animals↗
PubMed1994

Interleukin-6, interferon-gamma, and phospholipid levels in the alveolar lining fluid of human lungs. Profiles in coal worker's pneumoconiosis and idiopathic pulmonary fibrosis.

Cytokines are widely involved in physiologic as well as immunoinflammatory and fibrosing processes of the lung. The aim of this work was to study, by bronchoalveolar lavage, two groups of human interstitial lung diseases (ILD) with fibrosing propensity (ie, idiopathic pulmonary fibrosis [IPF], n = 10; and coal worker's pneumoconiosis [CWP], n = 15). Patients were compared with nonsmoker control subjects (n = 20). Cellularity, proteins, and phospholipids were determined in the alveolar fluids. In addition, two cytokines (interleukin-6 [IL-6] and interferon-gamma [IFN-gamma]), which are presumed to possess respective antifibrotic and profibrotic activities, were measured in the respiratory tract. Compared with control subjects, IPF and simple CWP showed alveolar hypercellularity (p < 0.05) and relative lymphocytosis (p < 0.05). Both exhibited increased alveolar permeability (ie, increased albumin/urea ratio, p < 0.05), with enhanced IL-6 and decreased IFN-gamma in the alveolar spaces (p < 0.05). On the other hand, IPF displayed an associated polymorphonuclear alveolitis, enhanced alveolar epithelial lining fluid (AELF) volume and low surfactant phospholipid levels (p < 0.05 vs control), whereas simple CWP shared an exclusive lymphocytosis, normal AELF volume, and a surfactant lipid overflow (p < 0.05 vs control). Relationships among all of these parameters were found only between alveolar cellularity, neutrophils and IL-6 levels in the AELF of IPF (respectively, r = 0.85, p = 0.0009, and r = 0.89, p = 0.0006). In summary, common alterations of cellular and cytokine turnover were observed in IPF and simple CWP and may reflect activity of the antifibrotic fight in these diseased lungs. Surfactant phospholipid levels are likely to represent a specific disturbance among IPF and CWP, but no clear relationship with respect to the other parameters could be established for explaining the difference in time course outcome.

Adult↗
PubMed1986

The corrected collagen content in paraquat lungs.

Biochemical analysis of collagen in a fibrosing lung often betrays its collagen-rich appearance in histopathology. This is due to the liability of lung tissue to extreme change in weight or volume in the presence of edema, hemorrhage, or other lesions, producing a great error in the biochemical data obtained from it. On morphometry of arterial density in lung section, we established a method for calculating the degree to which a given lung is transformed from a standard state of expansion, according to which we may correct for the content of collagen per lung volume. This method was applied to 14 autopsy paraquat lungs with various grades of fibrosis. Increase in collagen was shown to begin at about the 20th day of intoxication and advance thereafter, a finding in good accordance with lung morphology. The longer the survival, the less uniform the intrapulmonary distribution of collagen; even a severely fibrosing lung retained non-fibrotic areas.

Adult↗
PubMed1989

Carborundum pneumoconiosis. Fibers in the mineral activate macrophages to produce fibroblast growth factors and sustain the chronic inflammatory disease.

Carborundum is a synthetic abrasive manufactured through fusion of high grade silica sand and finely ground carbon in an electric furnace at 2,400 degrees C. It had been considered an inert dust until recently. Two recent epidemiologic studies in Quebec have documented an excess of interstitial lung disease in plant workers and some 30 workers have received workman compensation. Histopathologic lesions have been described in four of the workers. To further investigate the carborundum pneumoconiosis, nine groups of eight sheep were exposed once in the tracheal lobe to either 100 ml saline, 100 mg latex beads in 100 ml saline, 100 mg graphite in 100 ml saline, 100 mg carborundum particles in 100 ml saline, 100 mg ashed carborundum particles in 100 ml saline, 100 mg of quartz (Minusil-5) in 100 ml saline, 100 mg crocidolite fibers in 100 ml saline, 100 mg carborundum fibers in 100 ml saline, and 100 mg ashed carborundum fibers in 100 ml saline solutions. The animals had BAL at two-month intervals and autopsy at month 8. The BAL analyses of cellularity, cytotoxicity and fibrogenicity, in association to necropsy histopathology, documented that all particles except for quartz were inert. The two-carborundum fiber samples produced a similar sustained nodular fibrosing alveolitis and crocidolite asbestos fibers produced a peribronchiolar fibrosing alveolitis of comparable severity. Thus, the major bioactive dusts in the carborundum manufacturing process are quartz particles and the carborundum fibers generated in the process. The latter have fibrogenic activities comparable to asbestos fibers of similar size and are likely to contribute to the pathogenesis of the interstitial lung disease of carborundum workers.

Animals↗
PubMed2003

Aristolochic acid and 'Chinese herbs nephropathy': a review of the evidence to date.

Chinese herbs nephropathy (CHN) is a rapidly progressive interstitial nephropathy reported after the introduction of Chinese herbs in a slimming regimen followed by young Belgian women. It is characterised by early, severe anaemia, mild tubular proteinuria and initially normal arterial blood pressure in half of the patients. Renal histology shows unusual extensive, virtually hypocellular cortical interstitial fibrosis associated with tubular atrophy and global sclerosis of glomeruli decreasing from the outer to the inner cortex. Urothelial malignancy of the upper urinary tract develops subsequently in almost half of the patients. Suspicion that the disease was due to the recent introduction of Chinese herbs in the slimming regimen was reinforced by identification in the slimming pills of the nephrotoxic and carcinogenic aristolochic acid (AA) extracted from species of Aristolochia. This hypothesis was substantiated by the identification of premutagenic AA-DNA adducts in the kidney and ureteric tissues of CHN patients. Finally, induction of the clinical features (interstitial fibrosis and upper urothelial malignancy) typical of CHN in rodents given AA alone removed any doubt on the causal role of this phytotoxin in CHN, now better called aristolochic acid nephropathy (AAN). AAN is not restricted to the Belgian cases. Similar cases have been observed throughout the world, but AA is sometimes incriminated on the basis of the known content of AA in the herbs. The possibility remains that in some individuals in whom AA has not been demonstrated, other phytotoxins might be implicated. Biological and morphological features of AAN are strikingly similar to those reported in another fibrosing interstitial nephropathy of still unknown aetiology, Balkan endemic nephropathy (BEN). Interestingly, AA was incriminated as the cause of BEN many years ago, a hypothesis yet to be fully explored. The intake of AA and the presence of tissular AA-DNA adducts in patients with an unequivocal diagnosis of BEN remains to be demonstrated. The tragic phenomenon of CHN, recognised only 10 years ago, has been at the root of significant research and progress both in nephrology and oncology. It has provided a fascinating opportunity to understand the link between a fibrosing interstitial nephropathy and urothelial carcinoma. It allows the categorisation of interstitial nephritis on the basis of histological findings, of initiating toxic substances and of associated clinical features. Finally, it has led to the withdrawal in several countries of a previously unsuspected carcinogenic and nephrotoxic substance.

Animals↗
PubMed1998

Arterial and mixed venous oxygen desaturation during incremental exercise in patients with chronic pulmonary disease.

We evaluated arterial and mixed venous oxygen desaturation during symptom-limited exercise in patients with chronic pulmonary disease. Patients were divided into five groups according to disease: [chronic pulmonary emphysema (CPE), chronic bronchitis (CB), pulmonary tuberculosis sequalae (TB-seq), fibrosing lung disease (FLD), and pulmonary vascular disease (PVD)]. There were no significant difference in the values of arterial (PaO2) and mixed venous (PvO2) oxygen tension before and at the end of exercise among the five groups, whereas absolute decreases in PvO2 were significantly larger in PVD and FLD. The changes in PvO2 were similar to the changes in the coefficient of oxygen delivery (COD) which is equal to oxygen transport divided by oxygen consumption. These results suggest that the relative decrease in oxygen transport during exercise due to the high ratio of oxygen extraction by tissues is an important factor to determine decreases in PvO2 in pulmonary hypertensive disease and fibrosing lung disease.

Aged↗