Mediators of Inflammation

Mediators of Inflammation / 2002 / Article

Open Access

Volume 11 |Article ID 106591 |

Barbara Proust, Ghislaine Lacroix, Franck Robidel, Maryse Marliere, Anthony Lecomte, B. Boris Vargaftig, "Interference of a short-term exposure to nitrogen dioxide with allergic airways responses to allergenic challenges in BALB/c mice", Mediators of Inflammation, vol. 11, Article ID 106591, 10 pages, 2002.

Interference of a short-term exposure to nitrogen dioxide with allergic airways responses to allergenic challenges in BALB/c mice


Nitrogen dioxide (NO2) is a common indoor and outdoor air pollutant whose role in the induction of asthma is unclear. We investigated the effects of NO2 on the development of asthma-like responses to allergenic challenge in BALB/c mice. Ovalbumin (OVA)-immunized mice were intranasally challenged with OVA or saline solution just before starting a 3 h exposure to 5 or 20 ppm NO2 or air. Twenty parts per million of NO2 induced a significant increase of bronchopulmonary hyperreactivity in OVA-challenged mice and of permeability according to the fibronectin content of the bronchoalveolar lavage fluid (BALF) 24 h after exposure, as compared with air or 5 ppm NO2. Eosinophilia (cell counts in the BALF and eosinophil peroxidase of lung tissue) was detected at 24 and 72 h with similar levels for air and 20 ppm NO2, whereas a marked reduction was unexpectedly observed for 5 ppm NO2. At 24 h, interleukin-5 in the BALF was markedly reduced at 5 ppm compared with 20 ppm NO2 and was also more intense for 20 ppm NO2 than for the air group. In contrast to specific IgG1 titers, anti-OVA IgE titers and interleukin-4 in the BALF were not affected by NO2 exposure. Irrespective of the concentration of NO2, OVA-challenged mice did not develop late mucosal metaplasia compared with those exposed to OVA-air. These results indicate that a short exposure to NO2 can exacerbate or inhibit some features of the development of allergic disease in mice and may depend on the concentration of pollutant.

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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