Innate Lymphoid Cell–Dependent Airway Epithelial and Inflammatory Responses to Inhaled Ozone: A New Paradigm in Pathogenesis. (December 2019)

• Record Type: Journal Article
• Authors: Harkema, Jack R.; Wagner, James G.
• Other Names: Rao Deepa guest-editor.; Harkema Jack guest-editor.; Wolf Jeffrey guest-editor.
• Is Part Of: Toxicologic pathology. Volume 47:Number 8(2019)
• Page Start: 993
• Page End: 1003
• Publication Date: 2019-12
• Subjects: ozone -- mice -- rats -- monkeys -- mucous cell metaplasia -- eosinophils -- innate lymphoid cells -- nonallergic rhinitis and asthma; Pathology -- Periodicals; Toxicology -- Periodicals; Pathology; Toxicology; 615.9
• DOI: 10.1177/0192623319873872
• Languages: English
• ISSNs: 0192-6233

Abstract

Epidemiological associations have been made between the new onset of childhood rhinitis/asthma and exposures to elevated ambient levels of ozone, a commonly encountered gaseous air pollutant. Our laboratory was the first to find that mice repeatedly exposed to ozone develop nasal type 2 immunity and eosinophilic rhinitis with mucous cell metaplasia. More recently, we have found that these ozone-induced upper airway alterations are mediated by group 2 innate lymphoid cells (ILC2s) and not by T and B cells that are important in adaptive immune responses typically associated with allergic rhinitis and asthma. Furthermore, repeated exposures of mice to ozone cause ILC2-mediated type 2 immunity and airway pathology in the lungs, like those found in the nasal airways. Our recent findings in ozone-exposed mice complement and extend previous reports of nonallergic nasal airway disease in ozone-exposed rats and nonhuman primates. Overall, these experimental results in laboratory animals suggest a plausible ILC2-dependent paradigm for the toxicologic pathobiology that underlies the development of nonallergic rhinitis/asthma in children who live in environments with repeated occurrences of high ambient concentrations of ozone.