Pulmonary effects of ozone and allergen exposure in the absence of surfactant protein-D in mice.

Ozone and allergen inhalation causes pulmonary inflammation and impairs lung function in mice. These effects are heightened in the absence of the immunosuppressive surfactant protein-D. Increased expression of inflammatory mediators is critical for the initiation of inflammation and impairment of lung function following ozone and allergen inhalation. An Affymetrix microarray was used to understand global changes in gene expression that occurred after ozone inhalation and/or allergen sensitization and challenge in the abscence of surfactant protein-D. Identification of the set of genes up and down regulated in response to ozone and/or allergen led us to study specific cellular inflammatory pathways. This study has important implications for the study of lung diseases like asthma. C57BL/6, Balb/c and SP-D-/- mice were sensitized and challenged with the allergen Aspergillus fumigatus (Af), then exposed to air or ozone for 2 hours. Mice were also exposed to air or ozone alone. Mice were euthanized and a single-cell suspension of whole lung homogenate was generated at 12 hours post air or ozone exposure, 24 hours post Af/12 hours post air or ozone, 96 hours post Af/12 hours post air or ozone, or 168 hours post Af/12 hours post air or ozone. Whole lung homogenate gene expression was studied via Affymetrix microarray.