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This Article Full Text Full Text (PDF) All Versions of this Article: 290/1/L144    most recent 00131.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Poynter, M. E. Articles by Janssen-Heininger, Y. Search for Related Content PubMed PubMed Citation Articles by Poynter, M. E. Articles by Janssen-Heininger, Y.

Nitrogen dioxide enhances allergic airway inflammation and hyperresponsiveness in the mouse

Departments of ¹Medicine, ²Pathology, and ³Civil and Mechanical Engineering, University of Vermont, Burlington, Vermont

Submitted 23 March 2005 ; accepted in final form 31 July 2005

In addition to being an air pollutant, NO₂ is a potent inflammatory oxidant generated endogenously by myeloperoxidase and eosinophil peroxidase. In these studies, we sought to determine the effects of NO₂ exposure on mice with ongoing allergic airway disease pathology. Mice were sensitized and challenged with the antigen ovalbumin (OVA) to generate airway inflammation and subsequently exposed to 5 or 25 ppm NO₂ for 3 days or 5 days followed by a 20-day recovery period. Whereas 5 ppm NO₂ elicited no pathological changes, inhalation of 25 ppm NO₂ alone induced acute lung injury, which peaked after 3 days and was characterized by increases in protein, LDH, and neutrophils recovered by BAL, as well as lesions within terminal bronchioles. Importantly, 25 ppm NO₂ was also sufficient to cause AHR in mice, a cardinal feature of asthma. The inflammatory changes were ameliorated after 5 days of inhalation and completely resolved after 20 days of recovery after the 5-day inhalation. In contrast, in mice immunized and challenged with OVA, inhalation of 25 ppm NO₂ caused a marked augmentation of eosinophilic inflammation and terminal bronchiolar lesions, which extended significantly into the alveoli. Moreover, 20 days postcessation of the 5-day 25 ppm NO₂ inhalation regimen, eosinophilic and neutrophilic inflammation, pulmonary lesions, and AHR were still present in mice immunized and challenged with OVA. Collectively, these observations suggest an important role for NO₂ in airway pathologies associated with asthma, both in modulation of degree and duration of inflammatory response, as well as in induction of AHR.

asthma; eosinophil; neutrophil; lung

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