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Biomedical subjects

B Wallaert

Publications and source records attributed to B Wallaert.

At least 217 records · Page 12Linked to original sources
PubMed1990

Lymphocyte-mediated inhibition of platelet cytotoxic functions during Hymenoptera venom desensitization: characterization of a suppressive lymphokine.

Recently, it has been shown that platelets, through a receptor for the Fc fragment of IgE, could be specially triggered by venom allergens in hypersensitivity to hymenoptera, generating cytocidal mediators toward Schistosoma mansoni larvae, and oxygen metabolites measured by chemiluminescence. After rush immunotherapy, a depressed platelet response was demonstrated to be associated with the production of lymphokine(s). Here we report the characterization of a factor present in supernatants of antigen-stimulated T cells from patients after hymenoptera venom desensitization which is able to inhibit platelet cytotoxic functions in a dose-dependent manner. The optimal inhibition was observed with supernatants obtained after T lymphocyte stimulated with 10(-5) micrograms venom allergen/ml. Once specifically produced the platelet-suppressive effect of lymphocyte supernatants was not antigen specific. The producing T cell subpopulation was identified as CD8+. This lymphokine had an approximate molecular mass of 25 kDa and a pI of 4.8. It was heat and acid stable and sensitive to trypsin and proteinase K but not to neuraminidase. This platelet inhibitory activity was absorbed by platelet membrane suggesting its binding to a receptor. These properties were very similar to a previously described platelet activity suppressive lymphokine, suggesting the participation of this lymphokine in the mechanisms of rush desensitization.

Animals↗
PubMed1990

Subclinical alveolitis in immunologic systemic disorders.

Subclinical alveolitis is a frequent finding in immunologic systemic disorders. However the significance of subclinical alveolar inflammation does not seem to be univocal and varies according to the disease. The fact that pulmonary involvement is rare during the course of extrathoracic granulomatosis like Crohn's disease or primary cirrhosis and that subclinical alveolitis is frequent suggests that alveolar inflammation may be the expression in the lung of a systemic immune disorder. In contrast subclinical alveolitis in collagen-vascular diseases, particularly progressive systemic sclerosis, is frequently associated with abnormalities of lung parenchyma as assessed by CT scan supporting the hypothesis that subclinical alveolitis is associated with development of ILD. Close follow-up of these patients is needed to better determine whether subclinical alveolitis precedes ILD and whether early detection of subclinical alveolitis in immunologic systemic disorders may identify those patients that are at risk for the development of ILD in the future.

Autoimmune Diseases↗
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↗
PubMed1990

Short-term decrease of skin-test sensitivity after rush desensitization in Hymenoptera venom hypersensitivity.

Thirty-seven patients with a history of systemic anaphylactic stings were desensitized by the rush method. Patients were evaluated by skin testing twice, before and 6 weeks after desensitization. An additional control group of 10 patients, not yet desensitized, were tested for skin test technique reproducibility at 6-week intervals. Results were compared with IgE and IgG antibody levels, and with platelet reactivity towards specific Hymenoptera venom. Before desensitization, the maximum skin-test sensitivity was observed at 10(-5) micrograms venom/ml in 56% of patients and decreased to 10(-1) micrograms venom/ml after desensitization (48.6% of patients). Decrease of cutaneous tests was observed in 28/37 patients (75%) (P less than 0.001) and was not associated with significant variations of specific IgE or IgG antibody levels, but was correlated with the decrease of platelet reactivity (P less than 0.05). Conversely, variations of skin-test sensitivity in the control group was not significant.

Adolescent↗
PubMed1990

Superoxide anion generation by alveolar inflammatory cells in simple pneumoconiosis and in progressive massive fibrosis of nonsmoking coal workers.

We have examined superoxide anion (O2-) release by alveolar inflammatory cells recovered by bronchoalveolar lavage from the lower respiratory tract of 10 healthy nonsmokers and 25 nonsmoking pneumoconiotic patients, 11 with radiographic changes of simple pneumoconiosis (SP) and 14 with changes of progressive massive fibrosis (PMF). Significant increased number of cells was recovered from the lower respiratory tract from both patients with SP or with PMF. Alveolitis was made up predominantly of alveolar macrophages (AM) and an increased percentage of neutrophils in patients with PMF (3.3 +/- 0.7%). O2- release was evaluated using a superoxide dismutase (SOD)-inhibitable lucigenin-dependent chemiluminescence method. Spontaneous O2- generation by alveolar inflammatory cells from pneumoconiotic patients with SP was three to four times greater than that from 10 age-matched, healthy control subjects. O2- release by alveolar inflammatory cells from patients with PMF was dramatically increased when compared with that in patients with SP and with that in control subjects and was observed before and after stimulation by phorbol myristate acetate (PMA) (p less than 0.001). The increased O2- release was not due to a lack of enzyme antioxidant system within AM since intracellular superoxide dismutase was not lower in AM from patients than in AM from control subjects (p less than 0.05). Alteration of DLCO correlated with PMA-induced superoxide release by alveolar inflammatory cells in patients with PMF (p less than 0.05). Our data demonstrate that alveolar inflammatory cells from pneumoconiotic patients with PMF are in the activated state and release more oxygen-reactive species that do those from patients with SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Abnormal secretion of interleukin-1 and tumor necrosis factor alpha by alveolar macrophages in coal worker's pneumoconiosis: comparison between simple pneumoconiosis and progressive massive fibrosis.

The aim of this study was to compare the secretion of tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) by alveolar macrophages (AMs) harvested from patients with coal worker's pneumoconiosis (CWP) and control subjects. We observed higher levels of spontaneous TNF alpha and IL-1 secretion by AMs from patients with CWP than in those from healthy controls. We did not find any significant difference between the two groups in the incidence of simple pneumoconiosis and progressive massive fibrosis. In the group of coal miners without radiologic signs of pneumoconiosis, we found high levels of both cytokines in a subgroup of subjects still exposed to the mineral dust but not in the subgroup of subjects removed from exposure. These results indicate that AMs are involved in chronic lung inflammatory reactions to mineral dusts, partly by way of cytokine secretion. Moreover, cytokine secretion by AMs appears to be an early event that is detectable at the moment of mineral dust exposure. The results open new perspectives in the study of the mechanisms leading to CWP.

Bronchoalveolar Lavage Fluid↗
PubMed1990

Subclinical alveolitis in immunological systemic disorders. Transition between health and disease?

A subclinical inflammatory alveolitis as assessed by BAL cell analysis may be present in a high proportion of symptomless patients with immunological systemic disorders and with normal chest roentgenogram. Subclinical alveolitis can be characterized by the relative proportions of the different cell populations comprising the alveolitis and by the activated state of the cells. Thus, subclinical alveolitis can be classified into two major groups: lymphocyte and neutrophil alveolitis. Lymphocyte alveolitis is frequently found in patients with extrathoracic granulomatosis (Crohn's disease, primary biliary cirrhosis, extrathoracic sarcoidosis) or with some collagen vascular diseases (Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus). Neutrophil alveolitis is a main finding in collagen vascular diseases, especially progressive systemic sclerosis, dermatopolymyositis and mixed connective tissue disease. In addition, alveolar macrophages may be spontaneously activated and release various mediators that could be relevant to the pathogenesis of interstitial lung disease. On the other hand, some other alveolar macrophage functions (antibacterial activity may be severely impaired in some diseases, for example systemic lupus erythematosus). Alveolar inflammation is associated with an increase in the permeability of the alveolar membrane responsible for an increased influx of blood proteins in the alveolar spaces. Although subclinical inflammation may also be detected by high resolution computed tomography (HRCT) scan and/or lung permeability scintigraphic studies, the significance and prognostic value remains unclear and clearly differs according to both the disease and the pattern of alveolitis.

Humans↗
PubMed1990

Phagocyte enzymes in bronchoalveolar lavage from patients with pulmonary sarcoidosis and collagen vascular disorders.

The balance between proteases and antiproteases in the lower respiratory tract is believed to play a role in the outcome of interstitial lung diseases. In this cross-sectional study, we measure several phagocyte derived enzymes, namely plasminogen activator, neutrophil elastase and an ill-defined protease active on the trialanine chromophore substrate succinyl-alanine3-nitroanilide (SLAPN) in bronchoalveolar lavage (BAL) fluid from 42 patients with pulmonary sarcoidosis and from 43 patients with collagen vascular disease (CVD), 22 without lung disease (group I) and 21 associated with parenchymal lung disease (group II). The results show: a) that sarcoidosis is associated with increased plasminogen activator activity and with the presence of enzymatic activity against SLAPN corresponding at least in part to a metalloprotease; b) that CVD in the absence of radiographic lung disease is associated with an increase of plasminogen activator activity and increased levels of alpha 1-antiprotease-neutrophil elastase complexes; c) that the majority of untreated CVD (group II) patients have detectable levels of neutrophil elastase activity. These data show that patients with pulmonary sarcoidosis and CVD have different enzymatic profiles in their lower respiratory tract as assessed by BAL. Thus, sarcoidosis (mostly lymphocytic) is associated with enhanced macrophage-derived proteolytic activity in BAL, while CVD patients both with and without lung disease have increased neutrophil counts and neutrophil elastase complexed to alpha 1-protease inhibitor and presumably inactive in BAL. Finally, only BAL from untreated CVD patients with interstitial lung disease contain neutrophil elastase activity. This latter activity could contribute to the lung lesions frequently observed in these disorders.

Adult↗
PubMed1990

[Latent alveolitis in systemic disease. The transition between the normal and the pathological].

Alveolitis, an accumulation of inflammatory and immune cells in the alveolar structures, is the essential anatomical lesion associated with the development of pulmonary fibrosis. Broncho-alveolar lavage enables the detection of an alveolitis in patients without any respiratory disorder but having known pathology which can frequently lead to interstitial pneumonia, (certain systemic diseases). The cellular analysis of the bronchoalveolar lavage enabled two types of latent alveolitis to be identified: a lymphocytic alveolitis is very frequent during the course of extra-thoracic sarcoidosis, Crohn's disease, primary biliary cirrhosis, Sjögren-Gougerot syndrome, acute systemic lupus erythematosus and rheumatoid disease. A polymorphonuclear neutrophil alveolitis with or without an associated lymphocytosis which confirmed the almost exclusive attribute of either scleroderma, dermatopolymyositis or Sharp's syndrome. The role of alveolar macrophages is shown to be essential by the secretion of free oxygen radicals, chemotactic factor for polymorphonuclear neutrophils and for fibroblasts proliferation factors (fibronectin, fibroblastic growth factor). The significant and prognostic value of latent alveolitis remains poorly understood. A prolonged follow up of patients shows that the existence of a polymorpho-nuclear alveolar neutrophilia or of secretions containing fibronectin and free oxygen radicals from the alveolar macrophages is associated with a progressive deterioration of respiratory function. In summary the evidence of latent alveolitis in asymptomatic patients leads to the hope that in the future early therapeutic intervention may be instituted before the development of irreversible anatomical lesions.

Disease↗