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Published on: May 8, 2014
Ozone-Induced Models of Airway Hyperreactivity and Epithelial Injury
Michaela Albright1, Marissa A Guttenberg1, Robert M Tighe2
1Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, NC, USA.
Abstract:
Ozone (O3), a criterion air pollutant produced as a product of internal combustion, generates increased inflammation, lung permeability, and airway hyperreactivity when exposed to rodents in laboratory settings. Airway hyperreactivity is defined as an exaggerated acute obstructive response of the airways to one or more nonspecific stimuli. Lung permeability is a measure of barrier functions that separate internal and external environments to limit access of pathogens and other noxious material. By modeling in vivo O3 exposure in rodents, this allows investigators to explore pulmonary and nonpulmonary O3 effects as a means of understanding its impact on human health and lung function. Furthermore, direct effects of O3 on epithelial permeability can be defined using in vitro exposures to airway epithelial cells. This chapter will focus on methods of generating O3 and then exposing rodents and cultured epithelial cells in laboratory settings.
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