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Epinephrine is required for the IL‐13 induced increase in inflammatory cells in murine airways
Author(s) -
Thanawala Vaidehi Jatin,
Al-Sawalha Nour,
Forkuo Gloria Serwaa,
Omoluabi Ozozoma,
Knoll Brian,
Bond Richard
Publication year - 2012
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.26.1_supplement.668.2
Subject(s) - reserpine , mucus , inflammation , medicine , epinephrine , stimulation , cytokine , pharmacology , immunology , endocrinology , biology , ecology
Asthma is characterized by chronic inflammation of the lungs, including inflammatory cells migrating to the lungs, mucus production and airway hyper‐responsiveness. We have shown that in human bronchial epithelial cells, epinephrine (Epi) is required for mucus production in response to the inflammatory cytokine IL‐13. We treated mice with IL‐13 to study the role of Epi in the development of the asthma phenotype. Mice were administered reserpine (5 mg/kg i.p.) to pharmacologically deplete Epi. Reserpine treatment produced >99% reduction of adrenal Epi. We administered IL‐13, intra‐tracheally before or after reserpine treatment. IL‐13 treatment produces minimal inflammatory cells in the airways after 24 hours, with peak responses occurring at about 72 hours. Administration of reserpine prior to IL‐13 prevented the increase in inflammatory cells. However, administration of reserpine 24 hours after IL‐13 treatment did not prevent the increase in inflammatory cells. Thus depletion of Epi prior to stimulation with IL‐13 prevents inflammatory cells from reaching the lungs. However, administration of reserpine at a time point where little or no inflammatory cells are in the lungs does not prevent their accumulation following IL‐13 administration. These results suggest that Epi is required for the production or recruitment of inflammatory cells to the lungs. Supported by NIH 1R01A179236 to RAB