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Human Airway Epithelial Cells and Alveolar Macrophages Coordinate the Innate Immune Response to Acute Ozone Exposure
Author(s) -
Bauer Rebecca N,
Duncan Kelly,
DiazSanchez David,
Hernandez Michelle,
Jaspers Ilona
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.645.2
Subject(s) - innate immune system , ex vivo , cytokine , immune system , immunology , in vivo , bronchoalveolar lavage , chemistry , biology , medicine , lung , microbiology and biotechnology
Inhaled oxidant pollutants damage airway epithelial cells (EC) and induce cytokines and damage associated molecular patterns (DAMPs) to alert local immune cells and initiate an innate immune response. We examined how the interaction between EC and alveolar macrophages (AM) modifies innate immune responses to acute O 3 exposure. Healthy volunteers were exposed to 0.3 ppm O 3 or air for 2 hours. Bronchoalveolar lavage (BAL) was collected 1 hour post‐exposure and assessed for cytokines and DAMPs (ATP and uric acid). AM from the BAL were stimulated ex vivo with ATP and assessed for cytokine production. To model the EC‐AM interaction in vitro , AM from healthy volunteers were co‐cultured with ECs (16HBEo‐cell line). Co‐cultures, AM alone, and EC alone were exposed to 0.4 ppm O 3 or air for 4 hours and assessed for cytokine production 1 hour post‐exposure. We found acute O 3 exposure in vivo induced the release of interleukin (IL)‐8 and DAMPs, such as uric acid. At basal levels e x vivo, O 3 and air exposed AM produced similar amounts of IL‐8. With ex vivo ATP stimulation the O 3 , but not air, exposed AM had enhanced IL‐8 production, suggesting additional signals from the airway were necessary. Likewise, in vitro O 3 exposure of AM alone did not induce IL‐8 production, whereas AM‐EC co‐cultures had robust O 3 induced IL‐8 production. These results suggest the interaction between EC and AM is a key determinant of the innate immune response to O 3 .