Interference of a short-term exposure to nitrogen dioxide with allergic airways responses to allergenic challenges in BALB/c mice. Issue 4 (2002)
- Record Type:
- Journal Article
- Title:
- Interference of a short-term exposure to nitrogen dioxide with allergic airways responses to allergenic challenges in BALB/c mice. Issue 4 (2002)
- Main Title:
- Interference of a short-term exposure to nitrogen dioxide with allergic airways responses to allergenic challenges in BALB/c mice
- Authors:
- Proust, Barbara
Lacroix, Ghislaine
Robidel, Franck
Marliere, Maryse
Lecomte, Anthony
Vargaftig, B. Boris - Abstract:
- Abstract : 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 ofAbstract : 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. … (more)
- Is Part Of:
- Mediators of inflammation. Volume 11:Issue 4(2002)
- Journal:
- Mediators of inflammation
- Issue:
- Volume 11:Issue 4(2002)
- Issue Display:
- Volume 11, Issue 4 (2002)
- Year:
- 2002
- Volume:
- 11
- Issue:
- 4
- Issue Sort Value:
- 2002-0011-0004-0000
- Page Start:
- 251
- Page End:
- 260
- Publication Date:
- 2002
- Subjects:
- Inflammation -- Mediators -- Periodicals
Biological response modifiers -- Periodicals
Inflammation (Pathologie) -- Médiateurs
Immunomodulateurs
Biological response modifiers
Inflammation -- Mediators
Immunology
Autacoids
Immunologic Factors
Cell Adhesion Molecules
Cell Communication
Cytokines
Inflammation
Periodicals
Electronic journals
616.0473 - Journal URLs:
- https://www.hindawi.com/journals/mi/ ↗
- DOI:
- 10.1080/096293502900000113 ↗
- Languages:
- English
- ISSNs:
- 0962-9351
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 10173.xml