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Biomedical subjects

B Wallaert

Publications and source records attributed to B Wallaert.

At least 181 records · Page 10Linked to original sources
PubMed1993

T and B cell immune response to a 55-kDa endothelial cell-derived antigen in severe asthma.

Current concepts on the pathogenesis of chronic asthma emphasize the role of several inflammatory cell populations and their respective mediators that interact in a complex network. However, beside inflammatory cells, lymphocytes are also present in asthmatic airways. Although little is known about their involvement in asthma, it has been suggested that lymphocytes may participate in the development of chronic inflammation either through lymphokine secretion or through antibody production. In this study, we describe circulating IgG autoantibodies, directed against a common 55-kDa antigen shared by platelets and cultured endothelial cells, and found in 34 out of 97 asthmatic patients. Among epidemiological, clinical and biological characteristics of these asthmatic patients, the anti-55-kDa antigen antibodies are mainly restricted to patients with negative cutaneous prick tests (p = 0.0014), and corticosteroid-dependent asthma (p = 0.0036). These antibodies were also detected in a few patients with autoimmune disorders like systemic lupus erythematosus (3/30) or rheumatoid arthritis (2/36). Both platelet and endothelial cell antigens were cross-reactive, had an isoelectric point between 8.0 and 9.0, were insensitive to reducing agents such as 2-mercaptoethanol, and were not present on either platelet or endothelial cell surface, as determined by immunostaining assay. [3H]Thymidine incorporation assay with peripheral blood mononuclear cells from patients in the presence or in the absence of 55-kDa antigen, purified from nitrocellulose sheets demonstrated a specific incorporation in 6 out of 13 patients with circulating anti-55-kDa antigen antibodies, with index values ranging from 12 to 3. Such a T cell reactivity has also been observed in 3 out to 17 patients without detectable serum anti-55-kDa antigen antibodies. Moreover, a significant correlation was found between index values of antigen-specific T cell reactivity and the forced expiratory volume in one second (r = 0.544, p = 0.003). Our data indicate that the detection of such antibodies allows to distinguish a subgroup of asthmatics in terms of severity and to suggest a relationship between clinical severity and T and B cell autoreactivity to the 55-kDa platelet/endothelial cell antigen.

Adult↗
PubMed1993

Interleukin-6 and interleukin-1 alpha production is associated with antigen-induced late nasal response.

BACKGROUND: Cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 alpha, IL-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) are able to potentiate allergic inflammation and seem to be implicated in the development of the late allergic reaction. METHODS: To study the time course of cytokine production, sequential lavages were performed after nasal allergen challenge. Thirteen patients with allergic rhinitis and four healthy subjects were exposed to grass pollen (n = 6 and n = 2, respectively) or dust mite allergen (n = 7 and n = 2, respectively). RESULTS: Among the patients with allergic rhinitis, a single early response (single responders) developed in four, eight exhibited a dual response (dual responders) and one patient as well as the four healthy subjects did not respond. In addition to the measurement of IL-1 alpha, IL-6, TNF-alpha and GM-CSF concentrations by ELISA, the release of histamine, tryptase, and eosinophil cationic protein was also evaluated by radioimmunoassay performed on nasal lavage fluids. Concerning mediator levels in nasal lavage fluid, neither histamine release nor cytokine elevation were noted in healthy subjects. As previously described, histamine, tryptase and eosinophil cationic protein were released in single and dual responders. Concerning cytokines, TNF-alpha was undetectable in the majority of nasal lavages and an increase in GM-CSF concentration was occasionally observed whatever the type of response. In contrast, an increase in IL-1 alpha and IL-6 levels was observed for dual responders during the early period (12.6 +/- 3 and 9.2 +/- 2 pg/ml, respectively; p < 0.01 in both cases) and at a higher level during the late period (14.5 +/- 4, p not significant and 16.7 +/- 8 pg/ml, respectively; p < 0.01) when compared with baseline values (7.2 +/- 2.2 and 2 +/- 0.7 pg/ml, respectively). For single responders IL-1 alpha and IL-6 secretion was detected mainly during the early period. CONCLUSION: These data suggest a role for IL-1 alpha in the induction and perennisation of the inflammatory reaction in allergic rhinitis, whereas the role of IL-6 remains to be investigated.

Adult↗
PubMed1993

Pulmonary involvement in progressive systemic sclerosis: sequential evaluation with CT, pulmonary function tests, and bronchoalveolar lavage.

Computed tomographic (CT) findings obtained in 53 patients with progressive systemic sclerosis were correlated with functional parameters and bronchoalveolar lavage (BAL) results, and lung changes over time were assessed in 17 patients. CT findings were normal in 21 patients (group 1) with otherwise normal lung function, except for subclinical alveolitis in seven patients. CT depicted pleural and parenchymal abnormalities in 32 patients, grouped according to the absence (group 2) or presence (group 3) of honeycombing. In group 2 (n = 13), mean values of functional parameters were normal, and BAL showed a significant increase in neutrophils compared to group 1 (P < .05). Among patients in group 3 (n = 19) with limited extent of honeycombing (n = 12), the mean diffusing capacity value was lower in patients with a moderate ground-glass profusion score (n = 4) than in those with a mild score (n = 8) (68% +/- 4 [standard error of the mean] vs 80% +/- 3). CT is the method of choice for evaluating parenchymal destruction, and profusion and extent of ground-glass opacities can help in predicting the severity of lung damage in areas devoid of destructive changes.

Adolescent↗
PubMed1993

Subacute and chronic bird breeder hypersensitivity pneumonitis: sequential evaluation with CT and correlation with lung function tests and bronchoalveolar lavage.

PURPOSE: To evaluate lung involvement in the subacute (group 1) and chronic (group 2) stages of bird breeder hypersensitivity pneumonitis. MATERIALS AND METHODS: Computed tomographic (CT) findings in 45 patients were correlated with pulmonary function testing and bronchoalveolar lavage. Twenty-seven patients underwent sequential CT examination 0.3-4 years apart, with functional evaluation in 20 of them. RESULTS: In group 1, CT showed diffuse micronodules, ground-glass attenuation, focal air trapping or emphysema, and mild fibrotic changes, with normal lung volumes but impaired diffusing capacity and a predominant lymphocyte alveolitis. In group 2, two categories of chronic forms were identified at CT on the basis of presence or absence of honeycombing. After cessation of exposure, CT showed a return to normal or dramatic improvement in group 1 and considerable reduction in ground-glass attenuation and micronodules in group 2. CT depicted no fibrotic or emphysematous changes during follow-up. CONCLUSION: Subacute bird breeder hypersensitivity pneumonitis may share CT features with other types of hypersensitivity pneumonitis. CT may help in identification of emphysematous and fibrotic forms of chronic disease.

Acute Disease↗
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

Inactivation of alpha 1-proteinase inhibitor by alveolar inflammatory cells from smoking patients with or without emphysema.

The aim of this study was to evaluate the ability of alveolar inflammatory cells recovered by bronchoalveolar lavage from the lower respiratory tract of 17 smoking patients with or without emphysema to inactivate alpha 1-proteinase inhibitor (alpha 1-Pl). The presence of emphysema was determined and quantified using CT scan and was evidenced in 8 patients (Group 1), whereas 9 patients exhibited a normal CT scan (Group 2). Patients with emphysema had lower values of FEV1, DLCO, and resting PO2 and higher values of RV/TLC ratio than patients without emphysema. BAL analysis showed a higher percentage of neutrophils and of myeloperoxidase (MPO) in BAL fluid in Group 1 than in Group 2. Alveolar inflammatory cells stimulated or not with phorbol myristate acetate (PMA) were incubated for 45 min with purified alpha 1-Pl, and the results were expressed as a percentage of inactivation of alpha 1-Pl as evaluated by its inhibitory activity against porcine pancreatic elastase or human neutrophil elastase. In Group 2, unstimulated alveolar inflammatory cells inactivated only 3.3 +/- 0.7% alpha 1-Pl and stimulated cells inactivated only 5.4 +/- 1.1% alpha 1-Pl. In marked contrast, in Group 1, a significant loss of the antielastase function of alpha 1-Pl was observed (p < 0.001) when alpha 1-Pl was incubated with unstimulated cells (24.2 +/- 8.9%) or stimulated cells (35 +/- 8.9%) from Group 1. The addition of catalase to the cell suspension was associated with a significant decrease in the inactivation of alpha 1-Pl (from 35 +/- 8.9 to 10.2 +/- 1.2%, Group 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchoalveolar Lavage Fluid↗
PubMed1993

[Occupational extrinsic allergic alveolitis due to Aspergillus oryzae].

We report a case of extrinsic allergic alveolitis, provoked by Deterzyme, a product used in dermatology for the cleaning of cutaneous sores, and containing fractions of protolytic enzymes and amylases of Aspergillus oryzae. The diagnosis was based on the positive precipitins to an extract of antigen of the product as well as positive bronchial provocation tests (semi-delayed) and the disappearance of the symptomatology without any sequelae following cessation of exposure to the risk.

Alveolitis, Extrinsic Allergic↗
PubMed1993

[Chronic eosinophilic pneumonia or Carrington's disease].

Chronic eosinophilic pneumonia (CEP) was described by Carrington in 1969. It is twice as common in women as it is in men and is probably most common at middle age. Symptoms usually associated fever, weight loss, fatigue and dyspnoea. Extra-respiratory manifestations are rare but may involve many organs. Classical radiological findings are diffuse alveolar infiltrates, with a peripheral predominance which explains the classic description of a "negative of pulmonary edema". Peripheral blood eosinophilia is present in 90%. The inflammatory syndrome with an eosinophilic alveolitis is constant. Pulmonary function tests show a restrictive pattern with depressed DLCO and hypoxemia. In atypical cases, proof of diagnosis is supported by lung biopsies that show intra alveolar and interstitial accumulation of eosinophils in peripheral air spaces. Areas of bronchiolitis obliterans are also frequently seen. In some atypical forms of chronic eosinophilic pneumonia, other disorders have to be discussed, like bronchiolitis obliterans with an organizing pneumonia or cryptogenetic organizing pneumonia and even tuberculosis. After corticosteroid therapy, the resolution occurs very rapidly but relapses are frequent. Steroid-dependence is seen in 20 to 30% of patients.

Adrenal Cortex Hormones↗
PubMed1993

Bronchoalveolar lavage in allergic granulomatosis and angiitis.

Pulmonary involvement occurs in approximatively half of patients with allergic granulomatosis and angiitis (AGA). We studied bronchoalveolar cells from six patients with histologically proven AGA and compared our results with those obtained from four patients with chronic eosinophilic pneumonia (CEP), nine nonsmoking patients with bronchial asthma and blood eosinophilia, and 10 healthy nonsmokers. Pulmonary infiltrates were present in 5 out of 6 AGA patients. None of these patients was receiving corticosteroids at the time of entry to the study. Pulmonary function tests were normal in two cases, and demonstrated on obstructive ventilatory disorder with hypoxaemia in four cases. Total cell yield did not differ between AGA patients (22.4 +/- 4.9 x 10(4) cells.ml-1), asthmatics (9.6 +/- 1.7 x 10(4) cells.ml-1) and controls (11.3 +/- 1.5 x 10(4) cells.ml-1), whereas it was dramatically increased in patients with CEP (186.4 +/- 26.3 x 10(4) cells.ml-1). All six AGA patients demonstrated an increased percentage of alveolar eosinophils (mean: 31.1 +/- 9.9%; range 6-66%). In two patients evaluation of alveolar eosinophil subpopulations showed a low percentage (27 and 36%) of hypodense cells, when compared to the high levels (> 80%) found in CEP. No significant correlation could be established between bronchoalveolar (BAL) results and clinical data, pulmonary function abnormalities, or biological results. Sequential evaluation of alveolitis in two AGA patients undergoing corticosteroid therapy demonstrated persistent alveolar eosinophilia, despite disappearance of clinical, radiological and biological abnormalities. Our data demonstrate that eosinophils are present in the alveolar spaces of patients with AGA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Physiopathology of asthma].

Asthma is a multifactorial disease where genetic predisposition, environmental factors (allergens and pollutants) and endogenous factors intervene to varying degrees. Among the disturbances involved in the physiopathology of asthma dysfunction of the autonomic nervous system and development of bronchial inflammation are now known to play the major roles. From the adrenergic system, the role of which is now controverted, the attention of pharmacologists has shifted to the cholinergic central nervous system responsible for bronchial tone and the non adrenergic non cholinergic (NANC) nervous system. The more recently known NANC system is complex and mediated by neuropeptides, and it can alternately induce bronchodilatation and bronchoconstriction, as well as vasoconstriction and vasodilatation. The inhibitory NANC system acts through the bronchodilator VIP. The excitatory NANC system is mediated by tachykinins as which are potent bronchoconstrictors. Interaction of this system with the inflammatory cells induces a "neurogenic inflammation". Local inflammatory reaction is an almost constant element of asthma, irrespective of the cause of the disease. Although mast cells are the initial cells of the inflammatory reaction, there are important and complex cellular interactions with eosinophils, macrophages, lymphocytes and epithelial cells. Owing to their direct cytotoxic actions on the bronchial epithelium, eosinophils play a key-role in the inflammatory reaction. Cytokines secreted by alveolar macrophages, lymphocytes and mast cells amplify and maintain the inflammatory process.

Asthma↗
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

Levels of soluble IL-2 receptor in plasma from asthmatics. Correlations with blood eosinophilia, lung function, and corticosteroid therapy.

Evidence now suggests that eosinophils and T lymphocytes infiltrating bronchial tissues may play a key role in the pathophysiology of asthma. Circulating eosinophils, lung function, and plasma soluble IL-2 receptor (sIL-2R) were measured in 42 asthmatic patients referred for symptomatic asthma. The patients were divided into two groups based on the presence or absence of atopy. The group of non-atopic asthmatics was further divided according to the patients' requirement for long term oral corticosteroids. The mean sIL-2R +/- s.d. was 36.3 +/- 9.9 pM in the control group, 28.9 +/- 9.2 pM in the atopic asthmatics, 43.3 +/- 18.07 pM in the non-atopic asthmatics without oral steroid therapy, but was increased in the steroid-treated group (62.2 +/- 19.3 pM, P less than 0.01). A significant correlation was found between FEV1 and circulating eosinophils in atopic asthmatics and in non-atopic asthmatics without oral corticosteroid therapy, but not in the steroid-treated group. Furthermore, significant correlations were found between sIL-2R and FEV1, and between sIL-2R and blood eosinophils, in the group of non-atopic asthmatics not on oral steroid therapy. No such correlations were evidenced in the other groups of asthmatics. Similar results were obtained during the clinical course of three non-atopic patients followed for more than 1 year. These data suggest that T cell activation appears more prominent in non-atopic asthma than in atopic asthma. Moreover, it appears that T cell activation can occur in severe forms of asthma despite steroid treatment. Finally, the results suggest a possible link between T cell activation, eosinophils, and lung function, which may reflect a particular pathogenetic mechanism involved in non-atopic asthma.

Adrenal Cortex Hormones↗
PubMed1992

Increased pulmonary and intestinal permeability in Crohn's disease.

We tested the hypothesis that an increased epithelial permeability may affect sites other than the intestine in patients with Crohn's disease by simultaneously evaluating their pulmonary and intestinal permeability. Pulmonary and intestinal permeability were measured by clearance of inhaled technetium-99m diethylene triamine pentacetate (99mTc-DTPA) and by urinary recovery of chromium-51 ethylene diamine tetracetate respectively in 22 patients with Crohn's disease. The half time clearance of 99mTc-DTPA from lung to blood (t1/2LB) was decreased--that is pulmonary permeability increased--in the whole group of patients with Crohn's disease as compared with 13 controls (median 45.5 minutes (8-160) v 85 minutes (34-130) (p less than 0.003)). When analysed separately only patients with active Crohn's disease (n = 15) had a decreased t1/2 lung to blood v controls (42 minutes (8-160) v 85 minutes (34-130) (p less than 0.0025)). Among patients with active Crohn's disease, six were studied again when their disease was quiescent and their t1/2 lung to blood did not differ significantly. The intestinal permeability was increased in the whole group of Crohn's disease patients as compared with 15 controls (5.25% (1.2-24) v 1.7% (0.65-5.75) (p less than 0.0002)). When analysed separately both patients with active and inactive Crohn's disease had increased intestinal permeability v controls (8.1% (1.6-24) and 3.5% (1.2.9.2) v 1.7% (0.65-5.75)) (p less than 0.0001, p = 0.05 respectively). Six patients with active Crohn's disease were studied again when their disease was quiescent and their intestinal permeability decreased significantly p less than 0.04). Pulmonary permeability was increased in patients with Crohn's disease but was not greatly influenced by Crohn's disease activity as opposed to intestinal permeability. The mechanism of this increase is unknown, but may be related in some patients to the presence of an alveolitis.

Adolescent↗
PubMed1992

Increased intestinal permeability in active pulmonary sarcoidosis.

Altered permeability of the gut is a well-described feature in Crohn's disease. Because of pathologic similarities between Crohn's disease and sarcoidosis, we initiated this study to evaluate the permeability of the gut mucosal lining in patients with pulmonary sarcoidosis. A group of 18 patients with biopsy-proven pulmonary sarcoidosis (active n = 8, inactive n = 10) were included in the study. Control groups included 22 patients with Crohn's disease (active n = 12, inactive n = 10), nine untreated patients with recent pulmonary tuberculosis, six patients with coal worker's pneumoconiosis (CWP), eight patients with idiopathic pulmonary fibrosis (IPF), and 16 healthy subjects. All were nonsmokers. The 24-h urinary excretion of 100 microCi 51Cr-ethylenediaminetetraacetic acid (51Cr-EDTA) was used to test the intestinal permeability (IP). As previously demonstrated, patients with active Crohn's disease demonstrated a dramatic increase in IP (7.7 +/- 1.4%) that was clearly reduced in inactive CD (2.34 +/- 0.54%). Patients with active pulmonary sarcoidosis exhibited a marked increased IP to 51Cr-EDTA (4 +/- 0.54%), which was not found in patients with inactive sarcoidosis (1.6 +/- 0.17%). IP was normal in patients with pulmonary tuberculosis (1.03 +/- 0.25%), CWP (2.1 +/- 0.54%), and IPF (1.9 +/- 0.33%) and did not differ from the control group (1.76 +/- 0.23%). In addition, in 6 patients with active pulmonary sarcoidosis, the concentrations of albumin and hyaluronan were measured in jejunal perfusion fluid and compared with those obtained from 10 patients with active Crohn's disease and 16 control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1992

Long-term prognosis of near-fatal asthma. A 6-year follow-up study of 145 asthmatic patients who underwent mechanical ventilation for a near-fatal attack of asthma.

The objective of the present study was to investigate the long-term prognosis of near-fatal asthma. A retrospective cohort study design was used. Cases were defined as any asthmatic individual requiring mechanical ventilation for the first time for an asthma exacerbation between January 1, 1983 and December 31, 1988. The consecutive sample of patients was drawn from four study sites, specifically four intensive care units (ICU), based in a large urban area (1 million inhabitants). These four ICU total approximately 5,000 admissions per year and are the referral centers for more than 95% of patients requiring respiratory intensive care in the area. Data collection was obtained by questionnaires addressed to the patients and to their attending physicians and was completed by telephone calls if necessary. A total of 147 patients entered the study. The long-term outcome could be evaluated in all but two patients. The follow-up period ranged from 1 to 75 months. In-hospital mortality was 16.5%. Among the 121 patients discharged from the ICU, 18 subsequently died, 17 of whom died from a new attack of asthma. Post-hospitalization mortality was 10.1% (95% CI, 5.9 to 16.8%) after 1 yr, 14.4% (CI, 9 to 22.3%) after 3 yr, and 22.6% (CI, 12.7 to 36.8%) after 6 yr. Nearly two-thirds (61.5%) of these secondary deaths occurred within the year following discharge from the ICU. Smoking was associated with a higher in-hospital mortality, as well as with a higher posthospitalization mortality. Age was also independently associated with a higher posthospitalization mortality. It is noteworthy that the secondary deaths were mostly observed in patients over 40 yr of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗