Effect of ozone exposure on allergic sensitization and airway inflammation induced by dendritic cells

• Published in: Clinical and experimental allergy 2002-03, Vol.32 (3), p.391-396
• Main Authors: Depuydt, P. O., Lambrecht, B. N., Joos, G. F., Pauwels, R. A.
• Format: Article
• Language: English
• Subjects: 6 mice; Air Pollutants - adverse effects; Air Pollutants - immunology; airway inflammation; Allergic diseases; Animals; Antigen-Presenting Cells - immunology; Biological and medical sciences; Bronchoalveolar Lavage Fluid - cytology; Bronchoalveolar Lavage Fluid - immunology; C57Bl; Cell Movement; dendritic cell; Dendritic Cells - immunology; Dendritic Cells - metabolism; Disease Models, Animal; Dose-Response Relationship, Immunologic; Immunization; Immunopathology; Inflammation - etiology; Inflammation - immunology; Inflammation - pathology; Lung - blood supply; Lung - cytology; Lung - immunology; Male; Medical sciences; Mice; Mice, Inbred C57BL; Ovalbumin - adverse effects; Ovalbumin - immunology; Oxidants, Photochemical - adverse effects; ozone; Ozone - adverse effects; Ozone - immunology; Respiratory and ent allergic diseases; Respiratory Hypersensitivity - etiology; Respiratory Hypersensitivity - immunology; Respiratory Hypersensitivity - pathology; sensitization
• ISSN: 0954-7894; 1365-2222
• DOI: 10.1046/j.1365-2222.2002.01364.x

Background Epidemiological studies suggest that ozone exposure is related to increased asthma symptoms. Dendritic cells (DCs) are the principal antigen‐presenting cells in the airways. Objective We have examined whether ambient doses of ozone (100 ppb for 2 h) enhance allergic sensitization and/or airway inflammation in a mouse model. Methods C57BL/6 mice were sensitized to inhaled ovalbumin (OVA) by intratracheal instillation of OVA‐pulsed DCs on day 0. Daily exposure to OVA aerosol on days 14–20 resulted in an eosinophilic airway inflammation, as reflected in bronchoalveolar lavage fluid and lung histology. In a first experiment, mice were exposed to ozone or room air immediately prior to and following sensitization. Subsequently, we tested the effect of ozone exposure during antigen challenge in DC‐sensitized mice. Results Exposure to ozone during sensitization did not influence airway inflammation after subsequent allergen challenge. In contrast, in sensitized mice, challenge with OVA together with ozone (days 14–20) resulted in enhanced airway eosinophilia and lymphocytosis, as compared with mice exposed to OVA and room air (1.91 × 106 ± 0.46 × 106 vs. 0.16 × 106 ± 0.06 × 106 eosinophils/mL lavage fluid; P = 0.015; 0.49 × 106 ± 0.11 × 106 vs. 0.08 × 106 ± 0.03 × 106 lymphocytes/mL lavage fluid; P = 0.004). Ozone exposure without subsequent OVA exposure did not cause airway inflammation. Conclusion Ozone exposure does not increase allergic sensitization but enhances antigen‐induced airway inflammation in mice that are sensitized via the airways.