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  Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma

Klaßen, C., Karabinskaya, A., Dejager, L., Vettorazzi, S., Van Moorleghem, J., Lühder, F., et al. (2017). Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma. Journal of Immunology, 199(1), 48-61. doi:10.4049/jimmunol.1601691.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0000-8119-2 Version Permalink: http://hdl.handle.net/21.11116/0000-0000-811A-1
Genre: Journal Article

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 Creators:
Klaßen, C., Author
Karabinskaya, A., Author
Dejager, L., Author
Vettorazzi, S., Author
Van Moorleghem, J., Author
Lühder, F., Author
Meijsing, S. H.1, Author              
Tuckermann, J. P., Author
Bohnenberger, H., Author
Libert, C., Author
Reichardt, H. M., Author
Affiliations:
1Mechanisms of Transcriptional Regulation (Sebastiaan H. Meijsing), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479641              

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 Abstract: Although glucocorticoids (GCs) are a mainstay in the clinical management of asthma, the target cells that mediate their therapeutic effects are unknown. Contrary to our expectation, we found that GC receptor (GR) expression in immune cells was dispensable for successful therapy of allergic airway inflammation (AAI) with dexamethasone. Instead, GC treatment was compromised in mice expressing a defective GR in the nonhematopoietic compartment or selectively lacking the GR in airway epithelial cells. Further, we found that an intact GR dimerization interface was a prerequisite for the suppression of AAI and airway hyperresponsiveness by GCs. Our observation that the ability of dexamethasone to modulate gene expression in airway epithelial cells coincided with its potency to resolve AAI supports a crucial role for transcriptional regulation by the GR in this cell type. Taken together, we identified an unknown mode of GC action in the treatment of allergic asthma that might help to develop more specific therapies in the future.

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Language(s): eng - English
 Dates: 2017-05-172017-07-01
 Publication Status: Published in print
 Pages: 14
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: DOI: 10.4049/jimmunol.1601691
ISSN: 1550-6606 (Electronic)0022-1767 (Print)
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Title: Journal of Immunology
Source Genre: Journal
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Publ. Info: Bethesda, USA : American Association of Immunologists
Pages: - Volume / Issue: 199 (1) Sequence Number: - Start / End Page: 48 - 61 Identifier: ISSN: 0022-1767
ISSN: 1550-6606
CoNE: /journals/resource/0022-1767