Journal
INHALATION TOXICOLOGY
Volume 23, Issue 5, Pages 268-276Publisher
INFORMA HEALTHCARE
DOI: 10.3109/08958378.2011.566898
Keywords
Traffic-related air pollution; nitrogen dioxide; diesel exhaust particles; lung inflammation; allergic sensitization; intranasal mouse model
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Funding
- Norwegian Research Council [165422/v40]
- Norwegian Institute of Public Health
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The role of traffic-related air pollution in the development of allergic diseases is still unclear. We therefore investigated if NO(2), an important constituent of traffic-related air pollution, promotes allergic sensitization to the allergen ovalbumin (OVA). We also examined if NO(2) influenced the allergy adjuvant activity of diesel exhaust particles (DEP). For this purpose, mice were exposed intranasally to OVA with or without DEP present, immediately followed by exposure to NO(2) (5 or 25 parts per million [ppm]) or room air for 4 h in whole body exposure chambers. Eighteen hours after the last of three exposures, the lungs of half of the animals were lavaged with saline and markers of lung damage and lung inflammation in the bronchoalveolar lavage fluid (BALF) were measured. Three weeks later, after intranasal booster immunizations with OVA, the levels of OVA-specific IgE and IgG2a antibodies in serum were determined. Both NO(2) (25 ppm) and DEP gave lung damage, measured as increased total protein concentration in BALF, whereas only NO(2) seemed to stimulate release of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha). In contrast, only DEP significantly increased the number of neutrophils. Furthermore, DEP in combination with OVA stimulated the production of serum allergen-specific IgE antibodies. NO(2), however, neither increased the production of allergen-specific IgE antibodies, nor influenced the IgE adjuvant activity of DEP. Thus, based on our findings, NO(2) seems to be of less importance than combustion particles in the development of allergic diseases after exposure to traffic-related air pollution.
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