PubMed Health⌕ Search

Biomedical subjects

A-B Tonnel

Publications and source records attributed to A-B Tonnel.

10 recordsLinked to original sources
PubMed2006

[Pulmonary disease in dental laboratory technicians].

INTRODUCTION: The manufacture of dental prostheses exposes the technician to inhalation of various potentially dangerous dusts (silica, hard metals, dental alloys and acrylic resins). BACKGROUND AND VIEWPOINT: Inhalation of dusts produced by the technician in the work place may lead to several respiratory disorders (pneumoconiosis, hypersensitivity pneumonitis, asthma, lung cancer). The continuous development of new materials leads to further manifestations of these disorders and justifies their notification, even in the absence of an accepted occupational disease. This step is taken inconsistently as many dental technicians are not salaried or insured. CONCLUSION: The seriousness of some of these disorders and the absence of effective treatment makes it important to develop effective methods of prevention for the protection of individuals and groups, and for early detection.

Dental Prosthesis↗
PubMed2005

Inflammatory events in severe acute asthma.

Severe acute asthma can be induced by different triggers, allergens, irritants, viruses, etc., which induce inflammation and provoke acute bronchoconstriction. Inflammatory cells, such as activated eosinophils and neutrophils identified in sputum and bronchial lavages (BL) in severe acute asthma from children and adults are associated with increased levels of IL-5, IL-8, and of proinflammatory mediators. Viruses, but also endotoxin or allergen exposure, are able to recruit neutrophils, via an IL-8 production by activated macrophages or epithelial cells. Together, these inflammatory mediators are responsible for the diffuse bronchial inflammation, which involve large and small airways. Activated T cells may also be related to the pathogenesis of severe asthma. An aberrant CD8+ T lymphocyte response in bronchi, with a cytotoxic activity has been associated with fatal asthma. Moreover, the persistence of inflammatory cells in bronchi, particularly neutrophils, which respond poorly to corticosteroids, could be in part responsible for the epithelial damage, the extensive mucus plugging, and the abnormalities of epithelial and endothelial permeability which are associated with severe acute asthma. Further studies are necessary to better identify the implication of this increased bronchial permeability in the persistence of high levels of airway resistance, particularly in patients with status asthmaticus.

Acute Disease↗
PubMed2005

Recombinant Mycobacterium bovis BCG producing IL-18 reduces IL-5 production and bronchoalveolar eosinophilia induced by an allergic reaction.

BACKGROUND: Allergic reactions occur through the exacerbated induction of a Th2 cell type expression profile and can be prevented by agents favoring a Th1 profile. Bacillus Calmette-Guérin (BCG) is able to induce high IFN-gamma levels and has been shown to decrease experimentally induced allergy. The induction of IFN-gamma is mediated by interleukin (IL)-12 known to be secreted upon mycobacterial infections and can be enhanced by IL-18 acting in synergy with IL-12. OBJECTIVE: We evaluated the ability of a recombinant BCG strain producing IL-18 (rBCG) to modify the Th2 type responses in a murine model of ovalbumin (OVA)-dependent allergic reaction. METHODS: Mice were injected intraperitoneally or intranasally with OVA at days 0 and 15 and exposed to an OVA aerosol challenge at days 29, 30, 31 and 34. At days 0 and 15, two additional groups of mice received OVA together with 5 x 10(6) colony forming units of either rBCG or nonrecombinant BCG. RESULTS: A time-course analysis of OVA-specific immunoglobulin (Ig)E, IgG1 and IgG2a levels indicated no significant difference between the three groups of mice. However, following in vitro stimulation with OVA, lymph node cells from rBCG-treated mice produced less IL-5 and more IFN-gamma than those of mice injected with nonrecombinant BCG. In addition, 48 h after the last OVA challenge, a strong reduction of bronchoalveolar eosinophilia was found in the rBCG-injected mice compared to the nontreated or nonrecombinant BCG-treated groups. CONCLUSION: These results indicate that the production of IL-18 by rBCG may enhance the immunomodulatory properties of BCG that suppress pulmonary Th2 responses and, in particular, decrease airway eosinophilia.

Animals↗
PubMed2005

Allergic bronchopulmonary aspergillosis.

Allergic bronchopulmonary aspergillosis (ABPA) occurs in nonimmunocompromised patients and belongs to the hypersensitivity disorders induced by Aspergillus. Genetic factors and activation of bronchial epithelial cells in asthma or cystic fibrosis are responsible for the development of a CD(4)+Th2 lymphocyte activation and IgE, IgG and IgA-AF antibodies production. The diagnosis of ABPA is based on the presence of a combination of clinical, biological and radiological criteria. The severity of the disease is related to corticosteroid-dependant asthma or/and diffuse bronchiectasis with fibrosis. The treatment is based on oral corticosteroids for 6-8 weeks at acute phase or exacerbation and itraconazole is now recommended and validated at a dose of 200 mg/day for a duration of 16 weeks.

Aspergillosis, Allergic Bronchopulmonary↗
PubMed2004

[Efficacy and acceptability of the fixed fluticasone + salmeterol combination in the treatment of acute asthma attacks. Results of a one-year comparative study].

BACKGROUND: The objective of an asthma treatment is to control asthma, particularly to prevent exacerbations. OBJECTIVE: To study the efficacy, acceptability and safety of the fluticasone/salmeterol (FP/S) combination in preventing asthma exacerbations in comparison with the continuation of previous treatment (TA). METHODS: This was a multicentre, randomised, parallel-group study to compare the fixed combination FP/S to TA (treatment with a free combination of an inhaled corticosteroid and a long-acting beta2-agonist) over one year in patients whose asthma was well controlled with their current treatment. RESULTS: Five hundred and twenty patients were randomized and their data analyzed on an intent-to-treat basis. Seventy-four percent of the patients in the FP/S group and 71% in the TA group had no exacerbation. The 3.12% difference in favor of the FP/S group (90% CI: -3.32% to 9.56%) demonstrated that FP/S was at least as effective TA in preventing asthma exacerbations. Treatment acceptability, evaluated by the patient on visual analog scales (inclusion as part of the daily habits, constraint, simplicity) was better with FP/S (p<0.001) than with TA. Clinical safety was good and comparable in the two groups. CONCLUSION: The fixed fluticasone/salmeterol combination provided a protection as good as that obtained with free combinations over a one-year treatment period, with a significant improvement in treatment acceptability and a good clinical safety.

Adult↗
PubMed2004

[Involvement of dendritic cells in allergic airway diseases].

INTRODUCTION: Dendritic cells (DCs) are able to present antigen to T lymphocytes and to orientate the immune response towards a Th1 or a Th2 type. STATE OF THE ART: The aim of this report is to present different studies comparing DCs from allergic patients with those from healthy subjects using in vivo and in vitro experimental conditions. These studies have demonstrated that cellules dentritiquess from house dust mite allergic patients:i) take up house dust mite allergen more efficiently, ii) after stimulation by house dust mite allergen, secrete a restricted panel of cytokines and chemokines, and express characteristic co-stimulatory molecules, favoring a Th2 profile, iii) after stimulation by house dust mite allergen, induce Th2 cytokines secretion by T lymphocytes, and iv) favor an allergen-specific Th2 airway inflammatory response in an in vivo model of humanized mice. PERSPECTIVES: Functional modulation of DC could be a new therapeutic concept in allergic airway diseases. CONCLUSIONS: These results show phenotypic and functional specificities of DC from house dust mite allergic patients, and suggest a key-role for cellules dentritiques in the pathogenesis of allergen-dependent airway inflammatory response.

Dendritic Cells↗
PubMed2003

Keratinocyte growth factor (KGF) decreases ICAM-1 and VCAM-1 cell expression on bronchial epithelial cells.

Activation of leucocytes during airway inflammatory reaction involves adhesion to bronchial epithelial cells (BEC), a process implicating specific interactions between glycoproteins with epithelial cell surface proteins, mainly intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). In this study, the effect of keratinocyte growth factor (KGF), a growth factor involved in pulmonary epithelium repair, was evaluated on adhesion molecule expression with BEAS-2B cells and BEC and granulocyte adherence to BEAS-2B. The modulation by KGF of membrane and mRNA expression of ICAM-1 and VCAM-1 was studied on confluent cells stimulated or not with tumour necrosis factor-alpha (TNF) (200 UI/ml) or TNF and interleukin (IL)-4 (50 UI/ml and 10 ng/ml). Levels of soluble-(s)ICAM-1 and sVCAM-1 were measured by ELISA. Although moderately, KGF significantly decreased membrane ICAM-1 expression in unstimulated BEAS-2B cells (24% inhibition at 100 ng/ml) or in TNF- or TNF + IL-4-stimulated cells (22.5 and 18.7% inhibition, respectively). Treatment with KGF tended to decrease VCAM-1 expression in TNF- and TNF + IL-4-stimulated BEAS-2B (P = n.s. and P < 0.05, 14 and 15% inhibition, respectively). In primary culture of BEC, adhesion molecule expression was also reduced. ICAM-1 and VCAM-1 mRNA expression were also inhibited by KGF. Levels of sICAM-1 and sVCAM-1 were not significantly increased in supernatants from KGF-treated cells (30% and 24% increase at 100 ng/ml, respectively) compared to controls. Moreover, KGF decreased by 31% the adherence of neutrophils to TNF-activated BEAS-2B. In conclusion, KGF decreases ICAM-1 and VCAM-1 expression and neutrophil adherence in BEC. These suggest its involvement in the resolution of the inflammatory reaction.

Bronchi↗
PubMed2003

[Asthma in the elderly].

INTRODUCTION: Asthma in the elderly is a growing clinical problem. It affects 6 to 7% of this age-group, but making the distinction between asthma and chronic obstructive pulmonary disease is more difficult as patients get older. STATE OF THE ART: This difficulty is due to a number of factors: the confounding role of smoking, and also the physiological effects of ageing on the airways which renders airway obstruction more resistant to bronchodilation. Elderly asthmatics can be divided on clinical grounds into two arbitrary groups: "ageing asthmatics" who have had asthma since childhood or adolescence and "late-onset asthmatics" who may present following an infective episode. Certain features of asthma in the elderly include: poor perception of breathlessness, technical difficulties in making reliable pulmonary function measurements and the extra-pulmonary manifestations (impact on quality of life). PERSPECTIVES: The therapeutic strategy is much the same as for younger asthmatics but certain aspects take on greater importance: concerns about osteoporosis with long-term corticosteroid therapy (both oral and inhaled), the risk of arrhythmias with beta-2 adrenergic drugs and the significant side-effects of theophylline justifies, in difficult cases, consideration of anti-cholinergic and/or anti-leukotriene therapy. CONCLUSION: Most importantly, for elderly asthmatics it is a treatment regimen that is as simple as possible and is backed up by a written self-management plan that will improve outcomes.

Adolescent↗