[Effect of diesel particles on allergic inflammatory response: cellular targets and molecular mechanisms].
The prevalence of allergic diseases has increased in industrialized western countries, and several hypotheses have been proposed to explain this rise. Besides the classical "hygiene theory" associated with improvements in living standards, a role for atmospheric pollution has been suggested, but this has as yet not been proven by epidemiological studies. By contrast, the impact of pollutants on the allergic inflammatory response is well documented. In this context, the effects of diesel exhaust particles and their organic extracts are the best known. In both human and animal studies, it has been demonstrated that diesel exhaust particles can cause an augmentation of respiratory symptoms, which are associated with the development of mucosal inflammation, an increase in airways resistance, and the development of non-specific bronchial hyper-reactivity. The mechanisms of these airway modifications are better understood. Diesel exhaust particles interfere with several inflammatory cell-types, involved in the regulation of the immune response. Diesel particles act in synergy with antigens to selectively amplify the production of specific IgE, TH2 cytokines, chemokines, and to increase the expression of adhesion molecules. Diesel particles modify antigen presentation by the macrophage, and facilitate its interaction with T cell. Finally, diesel exhaust particles enhance mast cell and basophil histamine release, and might influence fibrotic bronchial remodeling. In essence, these data argue for an important role of such small respirable particles in the pathophysiology and, probably also, the epidemiological modification of allergic disease.
Devouassoux
G
G
Unité de Pneumologie, Département de Médecine Aiguë Spécialisée, Hôpital A. Michallon, CHU de Grenoble, France. GDevouassoux@chu-grenoble.fr
Brambilla
C
C
D000818:Animals; D001491:Basophils / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D005355:Fibrosis; D006632:Histamine / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E; D007249:Inflammation; D019570:Inhalation Exposure / Q000009:adverse effects*; D008407:Mast Cells / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology; D015533:Transcriptional Activation / Q000276:immunology; D001335:Vehicle Emissions / Q000009:adverse effects*
D018925:Chemokines; D016207:Cytokines; D001335:Vehicle Emissions; D007073:Immunoglobulin E; D006632:Histamine