Expression of Interleukin 9 in the Lungs of Transgenic Mice Causes Airway Inflammation, Mast Cell Hyperplasia, and Bronchial Hyperresponsiveness
Open accessAbstract
Interleukin (IL)-9, a pleiotropic cytokine produced by the Th2 subset of T lymphocytes has been proposed as product of a candidate gene responsible for asthma. Its wide range of biological functions on many cell types involved in the allergic immune response suggests a potentially important role in the complex pathogenesis of asthma. To investigate the contributions of IL-9 to airway inflammation and airway hyperresponsiveness in vivo, we created transgenic mice in which expression of the murine IL-9 cDNA was regulated by the rat Clara cell 10 protein promoter. Lung selective expression of IL-9 caused massive airway inflammation with eosinophils and lymphocytes as predominant infiltrating cell types. A striking finding was the presence of increased numbers of mast cells within the airway epithelium of IL-9–expressing mice. Other impressive pathologic changes in the airways were epithelial cell hypertrophy associated with accumulation of mucus-like material within nonciliated cells and increased subepithelial deposition of collagen. Physiologic evaluation of IL-9–expressing mice demonstrated normal baseline airway resistance and markedly increased airway hyperresponsiveness to inhaled methacholine. These findings strongly support an important role for IL-9 in the pathogenesis of asthma.
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Transgenic expression of Il9 results in allergic inflammation.
“Transgenic expression of Il9 results in allergic inflammation11–13.”
From The transcription factor PU.1 is required for the development of IL-9-producing T cells and allergic inflammation (2010) · cites this paper as [12]
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- Authors
- Temann, U.-A., Geba, G. P., Rankin, J. A., & Flavell, R. A.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Flavell, Richard A.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 1998-10-05
- Volume
- 188
- Issue
- 7
- Pages
- 1307-1320
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2212487
- OpenAlex
- W2139108455
- Cited by
- 452
- References
- 72
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 7 · 2023: 9 · 2022: 8 · 2021: 6 · 2020: 14 · 2019: 8 · 2018: 15 · 2017: 19 · 2016: 7 · 2015: 13 · 2014: 9 · 2013: 13 · 2012: 20
- FWCI
- 16.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Yale University (CT 06520)
- National Institutes of Health (5k04hl003229-05, HL-56389)
- Raymond and Beverly Sackler Institute for Biological, Physical and Engineering Sciences, Yale University
- National Heart, Lung, and Blood Institute (P01HL056389, R01HL054450, HL-03229, P50HL056389, HL-56389)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Keywords
- IL-9, asthma, airway inflammation, mast cell hyperplasia, airway hyperresponsiveness, transgenic mice, eosinophils, mucus hypersecretion, subepithelial collagen deposition, methacholine responsiveness, Th2 cytokines
- MeSH terms
- Animals, Bronchi, Epithelium, Female, Flow Cytometry, Histamine, Hyperplasia, Therapeutic Irrigation, Lung, Mast Cells, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Gene Expression, Bronchial Hyperreactivity, Interleukin-9, Mice, Rats
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