Ozone is an oxidant air pollutant in photochemical smog. Though nasal epithelial remodelling has been well-documented in laboratory animals repeatedly exposed to ozone, associated inflammatory responses have not been fully characterized. In this study, we investigated if the onset of ozone-induced nasal epithelial remodelling is related to temporal changes in granulocytic influx and cytokine gene expression. Mice exposed to 24-weekdays of ozone developed marked eosinophilic rhinitis with epithelial hyperplasia, mucous cell metaplasia and hyalinosis. Repeated subacute ozone exposures in mice induced an eosinophilic rhinitis with epithelial remodelling that resembled the pathology of human allergic/non-allergic rhinitis. Ozone-induced eosinophilic rhinitis was associated with an initial T helper cell 1 (Th1), followed by Th2-inflammatory response. Based on these findings, a study was conducted to investigate the role of lymphocytes (hypothesized cellular sources of Th1- and Th2-cytokines) in the development of eosinophilic rhinitis and associated nasal epithelial remodelling. In Rag2 x common gamma chain (γc) - deficient [RAG2(-/-) x γc(-/-)] mice, which lack T- and B- lymphocytes as well as NK cells, ozone nasal epithelial remodelling and eosinophilic rhinitis did not develop, hence supporting the hypothesis that lymphocytes are a crucial component to ozone induced eosinophilic rhinitis and associated epithelial changes in mice. These results suggest that chronic exposure to air pollutants, like ozone, may contribute to rising prevalence of allergic and non-allergic rhinitis.
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