Influx, Persistence, and Recall of Eosinophils and GATA-3+ Innate Lymphoid Cells in the Nasal Mucosa of Mice Exposed and Reexposed to the Gaseous Air Pollutant Ozone
Autor: | Jack R. Harkema, Ryan P. Lewandowski, Elyse A Eldridge, James G. Wagner |
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Rok vydání: | 2019 |
Předmět: |
Male
Ozone Mucous membrane of nose GATA3 Transcription Factor Toxicology Pathology and Forensic Medicine Persistence (computer science) 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Oxidants Photochemical Eosinophilic medicine Animals Lymphocytes Molecular Biology B cell 030304 developmental biology Rhinitis Pollutant 0303 health sciences Messenger RNA Air Pollutants Innate lymphoid cell Cell Biology Eosinophils Mice Inbred C57BL Nasal Mucosa medicine.anatomical_structure chemistry 030220 oncology & carcinogenesis Immunology |
Zdroj: | Toxicologic pathology. 48(2) |
ISSN: | 1533-1601 |
Popis: | Mice exposed to the air pollutant ozone develop eosinophilic rhinitis that is mediated by group 2, GATA-3+, innate lymphoid cells (ILC2s). In the present study, we determined the influx, persistence, and recall of nasal ILC2s and eosinophils in ozone-exposed mice. C57BL/6 (T/B cell sufficient, ILC sufficient), Rag2−/− (T/B cell deficient, ILC sufficient), and Rag2−/−Il2rg−/− (T/B cell deficient, ILC deficient) mice were exposed to 0 or 0.8 ppm ozone for 1 or 9 weekdays and killed 1 or 17 days postexposure. GATA-3+ lymphocytes were sparse in nasal tissue of air-exposed ILC-sufficient mice and absent in ILC-deficient mice. Nine-day, but not 1-day, ozone exposures induced nasal influxes of eosinophils and GATA-3+ lymphocytes in C57BL/6 and Rag2−/− mice but not in Rag2−/−Il2rg−/− mice. Eosinophils waned 17 days postexposure in ILC-sufficient strains of mice. GATA-3+ lymphocytes in C57BL/6 mice also attenuated after exposure but not in ILC-sufficient Rag2−/− mice. Eosinophils, but not GATA-3+ cells, increased rapidly with reexposure in ILC-sufficient mice. Type 2 immune-related messenger RNA expression correlated with cellular responses to ozone. These new findings in mice further elucidate the role of ILC2s in ozone-induced eosinophilic rhinitis and support epidemiologic associations between ozone exposure and eosinophilic inflammation in children. |
Databáze: | OpenAIRE |
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