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C Voisin

Publications and source records attributed to C Voisin.

At least 37 records · Page 2Linked to original sources
PubMed1995

Ozone stimulates synthesis of inflammatory cytokines by alveolar macrophages in vitro.

Ozone (O3) is one of the major irritant oxidant gases in photochemical smog. In the present study, the in vitro effect of low concentrations of O3 (0.1 to 1 ppm) was evaluated on cell viability and cytokine secretion by alveolar macrophages (AM) from guinea pigs and healthy subjects. Cell injury was estimated immediately after O3 exposure by evaluation of ATP cell content (measured by bioluminescence) and lactic dehydrogenase (LDH) release in the culture medium. No cytotoxic effect was found: the ATP cell content of both guinea pig AM and human AM did not significantly change after O3 exposure and similarly the LDH release in the culture medium was unchanged. AM-derived cytokines (tumor necrosis factor alpha [TNF alpha], interleukin-1 beta [IL-1 beta], interleukin-6 [IL-6], and interleukin-8 [IL-8]) were evaluated in AM supernatants. O3 exposure was associated with a significant increase in cytokine secretion, with a peak value at 0.4 ppm O3. The exposure of the guinea pig AM to 0.4 ppm O3 for 60 min increased the IL-6 activity by 252 +/- 60% and TNF activity by 202 +/- 35%. The increase in monokine production by the human AM was 443 +/- 208% for TNF alpha, 484 +/- 171% for IL-1 beta, 383 +/- 147% for IL-6, and 226 +/- 45% for IL-8 after a 60-min exposure to 0.4 ppm O3. Lowest O3 concentrations (0.1 and 0.2 ppm) only increased TNF alpha secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Asbestos-related rounded atelectasis. Radiologic and mineralogic data in 23 cases.

A retrospective study was conducted in 23 subjects with previous occupational exposure to asbestos and exhibiting rounded atelectasis (RA) on high-resolution computed tomography scan (HRCT scan) to evaluate the retention of asbestos bodies (ABs) using light microscopy in the bronchoalveolar lavage (BAL) fluid or lung parenchyma in such patients. A total of 31 RAs were identified, usually located in the lower (25 RAs) and posterior (23 RAs) parts of the lung. Pleural thickening in contact with the RA was observed in 27 RAs and parenchymal bands were detected in 15 cases. Twelve of the 20 patients who underwent BAL or surgery exhibited significant retention of ABs in BAL fluid or lung tissue. Moreover, a significant retention of ABs was observed in five of nine patients with a history of asbestos exposure but no diffuse pleural thickening on chest radiograph or interstitial opacities on HRCT scan. Patients with RAs and coexisting diffuse pleural thickening and/or interstitial fibrosis should be considered at a higher risk for lung cancer in comparison to patients with isolated circumscribed pleural plaques based on increased AB counts. By contrast, the excess risk of lung cancer is more questionable in patients with only RAs and circumscribed pleural plaques as they may have AB counts either above or below that associated with pleural plaques alone. This emphasizes the need for further follow-up studies to define criteria indicating the need for thoracotomy in these subjects.

Asbestos↗
PubMed1994

Ultrastructural and biochemical changes in alveolar macrophages exposed to nickel hydroxy carbonate.

The aim of this investigation was to assess the cytotoxic effect of nickel hydroxy carbonate (NiHC) on guinea pig alveolar macrophages (AMs) by studying ultrastructural modifications and by determining beta-glucuronidase (BG) and lactate dehydrogenase (LDH) activities, as well as cellular ATP content. The ultrastructural studies revealed phagocytosis of NiHC particles and a general vacuolisation of the cells, especially at high concentrations. X-ray microprobe analyses of these particles demonstrated the presence of Ni, P and Ca which suggests the formation of Ni-P-Ca complexes. In exposed cells, a biphasic change in intracellular ATP concentrations was observed which could indicate 'activation' of AMs at low concentrations and inhibition of energy generation at higher concentrations. As for enzymatic activities, a dose-dependent increase in LDH release was observed except at low doses which increased ATP. There was a good correlation between ATP decrease and LDH release, consistent with a dose-dependent cytotoxic effect of NiHC. However beta-glucuronidase activity remained unchanged at all NiHC concentrations. It has been concluded that NiHC undergoes an intracellular, biological transformation to form Ni-P-Ca. Further investigations are needed to determine the precise nature and importance of these complexes.

Adenosine Triphosphate↗
PubMed1994

Mechanisms of fibrosis in coal workers' pneumoconiosis. Increased production of platelet-derived growth factor, insulin-like growth factor type I, and transforming growth factor beta and relationship to disease severity.

To identify the clinical relevance of cytokines involved in the development of lung fibrosis observed in patients with coal workers' pneumoconiosis (CWP), we investigated the BAL fluid contents and AM secretions of three mediators that modulate fibroblast growth: platelet-derived growth factor (PDGF), Type I insulin-like growth factor (IGF-I), and transforming growth factor Type beta (TGF-beta). Our study population consisted of 25 patients with CWP (16 simple pneumoconiosis, SP, 9 progressive massive fibrosis, PMF, 9 control subjects, and 6 patients with idiopathic pulmonary fibrosis (IPF). The fibrotic potency of AM supernatants was also tested for their ability to promote the growth of a human lung fibroblast cell line appreciated by [3H]-thymidine incorporation. PDGF and IGF-I concentrations were increased in BAL fluids of patients with PMF compared with SP and control subjects, whereas TGF-beta concentration was significantly higher in BAL fluid of patients with SP compared with PMF and control subjects. PDGF, IGF-I, and TGF-beta concentrations in AM supernatants followed the same profile observed in BAL fluids, suggesting that AM is one of the main cell sources of PDGF, IGF-I, and TGF-beta in the lung of pneumoconiotic patients. After treatment by acidification, which activated the latent form of TGF-beta, AM from patients with SP induced an inhibition of [3H]-thymidine incorporation and fibroblast growth was restored after neutralization of TGF-beta by specific antibodies. In contrast, AM supernatants from patients with PMF and IPF promoted the proliferation of fibroblasts and treatment by acidification did not modify this effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Environmental airborne tremolite asbestos pollution and pleural plaques in Afghanistan.

A 51-year-old man underwent pleuroscopy for radiologic pleural abnormalities. Pathologic examination of pleural and lung biopsy specimens concluded on hyalinized pleural plaques associated with mild asbestosis. Transmission electron microscopy analysis showed significant retention of tremolite asbestos fibers. The absence of any occupational exposure to asbestos and the existence of geologic deposits of tremolite in the Kabul area of Afghanistan suggest an environmental exposure during the patient's childhood spent in this region.

Afghanistan↗
PubMed1993

Oxidative inactivation of alpha 1-proteinase inhibitor by alveolar epithelial type II cells.

The aim of this work was to evaluate the ability of guinea pig alveolar epithelial type II cells to generate significant amounts of reactive oxygen species to inactivate alpha 1-proteinase inhibitor (alpha 1-PI). Inactivation of alpha 1-PI was evaluated by its inhibitory activity against porcine pancreatic elastase and was expressed as a percentage. The same experiments were performed in parallel with alveolar macrophages (AM) obtained from the same animals and with MRC-5 fibroblasts. Both type II cells and AM released significant amounts of hydrogen peroxide and superoxide, whereas the fibroblasts did not. Unstimulated type II cells (0.5 +/- 2%), AM (1.2 +/- 1.5%), and fibroblasts (0.5 +/- 0.5%) were unable to inactivate alpha 1-PI. Addition of phorbol myristate acetate did not increase their ability to inactivate alpha 1-PI. In contrast, type II cells (79.7 +/- 7%) and AM (80.1 +/- 8%) dramatically inactivated alpha 1-PI in the presence of myeloperoxidase (25 mU/ml), whereas fibroblasts did not. Addition of catalase to the reaction significantly prevented the inactivation of alpha 1-PI. Western blot analysis of alpha 1-PI did not reveal a significant proteolysis of alpha 1-PI, which supports the hypothesis that, in the presence of neutrophil-derived myeloperoxidase, type II cells may oxidatively inactivate alpha 1-PI.

Animals↗
PubMed1993

Organization of home respiratory care: the experience in France with ANTADIR.

In France, home mechanical ventilation (HMV) is mainly organized through the public system, using a national network of 33 Regional Associations for home care of chronic respiratory insufficiency, which are federated on a national basis by The French National Home Care Association for Chronic Respiratory Insufficiency (ANTADIR). Twenty three thousand six hundred and twenty three patients were being treated at home through that organization at the end of 1991, 14,173 of whom received long-term oxygen therapy (LTO), 2,267 were ventilated by tracheostomy, 1,139 had nasal mask ventilation, and 3,322 received nasal continuous positive airway pressure (CPAP). In common practice, the association performs the installation of the respiratory apparatus at home, at no cost to the patient who is covered by the social security for all expenses. At the end of 1991, the total cost of home respiratory care delivered by ANTADIR rose to 78.6 millions US dollars.

France↗
PubMed1992

Effects of nickel hydroxycarbonate on alveolar macrophage functions.

The metabolic effects of different concentrations of nickel hydroxycarbonate (NiHC) on guinea pig alveolar macrophages (GPAMs) were investigated. Exposure to high concentrations of NiHC (6.25 and 12.5 micrograms 10(-6) cells) led to cell vacuolization. Morphological changes were associated with a dramatic reduction in the steady-state level of cellular adenosine triphosphate (ATP), i.e. ATP levels were reduced by 35% (P less than 0.001) and 53% (P less than 0.01), respectively. Low concentrations of NiHC (0.0625 and 0.125 microgram 10(-6) cells) did not induce morphological changes but increased cellular ATP content by 19% (P less than 0.01) and 12% (P less than 0.05), respectively. Effects of NiHC (0.125 and 6.25 micrograms 10(-6) cells) on cell oxidative metabolism were studied. The chemiluminescence was significantly increased (P less than 0.001) by the lower but not the higher concentration. A slight inhibition of total superoxide dismutase (P less than 0.05) and a decrease of catalase activity were demonstrated (P less than 0.05) for the high dose, while the low dose decreased the levels of reduced and total glutathione. In conclusion, the effects of NiHC on alveolar macrophages are characterized by an overproduction of free radicals for low concentrations and the depletion of cellular reserve energy, particularly ATP, for high concentrations.

Adenosine Triphosphate↗
PubMed1992

[Long-term tolerability of formoterol in chronic obstructive bronchopathies].

Formoterol aerosol, a long-acting new beta 2-mimetic was administered over a year at a dose of 12 micrograms twice daily, to 62 chronic obstructive bronchitics of mean age 66 +/- 6 years and of whom the basal VEMS was at 12,801 +/- 0.59. Clinical tolerance of the product was good with undesirable effects in 13 patients, the most frequent being shaking. No untoward effect was seen on systolic or diastolic arterial pressure, or the heart rate over successive visits at 1, 3, 6, 9 months and one year. Electrocardiographic surveillance found in only four patients electrical abnormalities that may be due to Formoterol, these were patients without previous cardiac problems but of advanced mean age. Functionally, a significant improvement of basal VEMS was noticed from the 6th month. The VEMS improved significantly after administration of 12 micrograms on successive visits, without tachyphylactic signs. Well tolerated, with functional benefits, Formoterol is a promising product amongst the long-acting beta 2-mimetics. Its usefulness and limitations in the basic treatment of these chronic bronchopathies remains to be defined.

Adrenergic beta-Agonists↗
PubMed1992

[Occupational dust exposure and chronic obstructive bronchopulmonary disease. Etiopathogenic approach to the problem of compensation in the mining environment].

In order to support the hypothesis of a causal relationship between exposure to respirable coal mine dusts and chronic obstructive pulmonary disease (COPD), investigations were performed to assess the biological disorders affecting the distal air spaces in coal workers with pneumoconiosis. Broncho alveolar lavage studies demonstrated a continual influx of mononuclear phagocytes loaded with mineral particles, associated with neutrophils in small number, in smokers as well as in non smokers. The alveolar macrophages were in activated state, spontaneously releasing various mediators, particularly interleukin I, Tumor necrosis factor alpha and superoxide anion. So, they appeared as responsible both for a chronic inflammation of the distal airways and for a protease-antiprotease imbalance leading to pulmonary emphysema, partly due to an oxidative inactivation of alpha 1 antiprotease inhibitor. In spite of additive effect of tobacco smoke, as shown by longitudinal studies of lung function in coal miners, it is now reasonable to consider the evidence of association between coal mine exposure and COPD to be sufficiently strong to infer causality, and to justify compensation for COPD in coal miners with or without radiological evidence of pneumoconiosis.

Coal↗
PubMed1991

Human alveolar macrophage antibacterial activity in the alcoholic lung.

Alcoholic individuals are predisposed to respiratory infections. However, mechanisms of perturbations leading to increased susceptibility to lung infections of individuals with alcoholic liver cirrhosis (ALC) are not fully understood. We studied the antibacterial activity and oxidant generation (before and after stimulation by phorbol myristate acetate or opsonized zymosan) of alveolar macrophages from 16 patients with ALC. Our results were compared with those obtained from 12 healthy control subjects, from 8 patients with primary biliary cirrhosis (PBC), and from 8 alcoholic individuals without cirrhosis. All were nonsmokers, had normal chest X-rays, and did not present evidence of lung infection 3 months before. The total number of cells recovered by bronchoalveolar lavage did not significantly differ between control subjects and patients. The cellular viability of alveolar macrophages (trypan blue exclusion) was greater than 90% in all cases. The antibacterial activity of alveolar macrophages versus Staphylococcus aureus was severely impaired in ALC (-21 +/- 8.2%) whereas it was normal in PBC (52 +/- 4.2%), in alcoholic subjects (44.6 +/- 5.4%), and in control subjects (60 +/- 5.5%). The same pattern of results was observed versus Escherichia coli (-47.7 +/- 10,28 +/- 8,28 +/- 12, and 29 +/- 8.5%, respectively). Previous incubation of normal alveolar macrophages with serum or BAL fluid from ALC patients or with normal serum or normal BAL fluid did not result in a significant decrease in antibacterial activity of normal alveolar macrophages. To distinguish ingested bacteria from adherent extracellular bacteria, cells that had been incubated with bacteria for 90 min were then incubated with lysostaphin (1 microgram/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Production of tumor necrosis factor-alpha and interleukin-6 by human alveolar macrophages exposed in vitro to coal mine dust.

Following our previous demonstration of cytokine secretion by alveolar macrophages (AM) from coal miners and from patients with coal workers' pneumoconiosis, we investigated the effect of in vitro exposure to coal dust and to its silica content on tumor necrosis factor-alpha (TNF), interleukin (IL)-1 beta, and IL-6 production by normal human AM. TNF and IL-1 beta concentrations were estimated by a specific radioimmunoassay, while IL-6 levels were evaluated by the proliferation of 7TD1 cells. After 24-h culture, coal dust triggered a significant release of TNF and IL-6 at the dose of 0.1 mg/ml and more obviously at 1 mg/ml in comparison with titanium dioxide (TiO2), used as a biologically inert control dust (with 1 mg/ml of dust: 3,526 +/- 3,509 versus 330 +/- 138 pg TNF/ml and 224 +/- 74 versus 72 +/- 34 U IL-6/ml, respectively; P less than 0.01 in both cases). After 3-h culture, a significant TNF secretion as well as an increased TNF mRNA expression were also detected for AM stimulated by coal dust at variance with TiO2. In contrast, no modification of IL-1 beta concentration could be evidenced in AM exposed to coal dust, although we detected an increased expression of specific mRNA expression. In order to define the role of silica among the main components of coal dust in AM activation, we evaluated the effect of silica (alpha-quartz, 30 micrograms/ml, which is the concentration and the type of silica present in our coal dust) alone or mixed with TiO2 (1 mg/ml) on monokine production.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1991

Oxidative inactivation of alpha 1-proteinase inhibitor by alveolar macrophages from healthy smokers requires the presence of myeloperoxidase.

The aim of this work was to study the ability of human alveolar macrophages (AM) of 10 healthy smokers to inactivate alpha 1-proteinase inhibitor (alpha 1PI). Purified alpha 1PI was incubated for 45 min, with human alveolar macrophages before and after stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. As a positive control, the same experiments were performed in parallel with blood human neutrophils (PMN). Results are expressed as percentage of inactivation of alpha 1PI as evaluated from its inhibitory activity against porcine pancreatic elastase. A strong correlation (r = 0.99) was shown when inhibitory activity of alpha 1PI was evaluated against porcine pancreatic elastase or human neutrophil elastase. Unstimulated AM (1.57 +/- 0.9%) as well as stimulated AM (PMA: 1 +/- 0.4%; zymosan: 3 +/- 0.6%) were unable to inactivate alpha 1PI. Gel electrophoresis of alpha 1PI demonstrated that AM before or after stimulation induced a slight proteolysis of alpha 1PI, whereas both cleaved and complexed alpha 1PI were found when alpha 1PI was incubated with activated PMN. Both unstimulated (22 +/- 2.6%) and activated PMN (PMA: 91.7 +/- 4.7%; zymosan: 90 +/- 5.5%) were responsible for a significant inactivation of alpha 1PI. Catalase, in contrast to superoxide dismutase, was responsible for a near complete protection of alpha 1PI inactivation by PMN. To better determine the role of PMN secretory products, especially myeloperoxidase (MPO), we also investigated the effect of zymosan-activated PMN supernatants or of purified MPO on the alpha 1PI-AM reaction. MPO assay in PMN supernatants demonstrated that activated neutrophils released significant amounts of MPO (16.8 +/- 4.1 U/ml), whereas MPO was undetectable in activated AM supernatants.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[In vivo kinetics of cotrimoxazole in alveolar macrophages].

The aim of this work was to study the kinetic of intramacrophage penetration of cotrimoxazole in guinea pigs which had received 100 mg/kg of sulfamethoxazole and 20 mg/kg of trimethoprim after a single intraperitoneal injection. 30 minutes, 1, 3, 6 and 24 hours after this injection an intra-cardiac blood sample was taken and pulmonary lavage was performed immediately after sacrificing the animal by cervical cord dislocation. The level of trimethoprim and sulfamethoxazole was measured in each sample by high performance liquid chromatography (HPLC). An estimation of the dilution of the supernatant was obtained by comparing the supernatant glucose with the serum glucose. The serum kinetics of trimethoprim and sulfamethoxazole progressed in a parallel fasion with time with a maximal concentration at 30 minutes (for trimethoprim: 6.7 +/- 0.9 micrograms/ml and for sulfamethoxazole 176.1 +/- 16.2 micrograms/ml). On the other hand their penetration capacity was different in the supernatant and in the alveolar macrophages: the maximal concentrations were obtained after one hour in the supernatant and after 3 hours in the cellular extract and were respectively for trimethoprim 0.43 +/- 0.07 microgram/ml and 20.9 +/- 8.06 micrograms/ml of intramacrophage water and for sulfamethoxazole 1.86 +/- 0.24 micrograms/ml and 23.8 +/- 12.7 micrograms/ml of intramacrophage water. A concentration around six times greater was noted for the trimethoprim inside the cells compared with serum and was only 0.25 time for sulfamethoxazole. On the other hand the supernatant/serum ratio showed a greater concentration for trimethoprim (4 to 10) than for sulfamethoxazole (0.6 to 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The penetration of co-trimoxazole into alveolar macrophages and its effect on inflammatory and immunoregulatory functions.

The pharmacokinetics of co-trimoxazole in serum, bronchoalveolar lavage-fluid (BAL-fluid) and alveolar macrophages (AM) of guinea pigs receiving sulphamethoxazole (100 mg/kg) and trimethoprim (20 mg/kg) were studied. HPLC showed that peak co-trimoxazole levels were obtained in serum at 30 min, in BAL-fluid at 1 h and in AM at 3 h. A comparison between mean concentrations in serum, BAL-fluid and AM showed a six-fold higher concentration of trimethoprim in cells than in serum, but only 0.25-fold of sulphamethoxazole. The BAL-fluid/serum ratio was four to ten times higher for trimethoprim than for sulphamethoxazole (0.6-to-one-fold). Sulphamethoxazole/trimethoprim ratios (30 min, 1 and 3 h) were lower in BAL-fluid (4.9 +/- 0.5) and in AM (1.4 +/- 0.5) than in serum (30.7 +/- 1.6). The influence of co-trimoxazole in vitro on microbicidal capacities (superoxide anion and hydrogen peroxide generations), immunoregulation (production of interleukin 1) and pro-inflammatory agent production (tumour necrosis factor) of guinea pigs' AM was also studied. No significant effect of co-trimoxazole on superoxide anion and hydrogen peroxide generations, or on interleukin 1 and TNF production, was demonstrable.

Animals↗