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.
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Authors | Jack R Harkema, James G Wagner |
Journal | Toxicologic pathology
(Toxicol Pathol)
Vol. 47
Issue 8
Pg. 993-1003
(12 2019)
ISSN: 1533-1601 [Electronic] United States |
PMID | 31537180
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S., Review)
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Chemical References |
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Topics |
- Air Pollutants
(toxicity)
- Animals
- Humans
- Immunity, Innate
(drug effects)
- Inhalation Exposure
(adverse effects)
- Lymphocytes
(drug effects, immunology, pathology)
- Metaplasia
- Ozone
(toxicity)
- Respiratory Mucosa
(drug effects, immunology, pathology)
- Respiratory Tract Diseases
(chemically induced, immunology, pathology)
- Species Specificity
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