IL-9 and its receptor in allergic and nonallergic lung disease: Increased expression in asthma
Open accessAbstract
Background Bronchial asthma is a chronic inflammatory disease associated with genetic components. Recently IL-9 has been reported as a candidate gene for asthma and to be associated with bronchial hyperresponsiveness and elevated levels of total serum IgE. Objective To investigate the contribution of IL-9 to the pathogenesis of asthma, we examined the expression of IL-9 and its receptor (IL-9R) in bronchial tissue from subjects with atopic asthma (n = 10), chronic bronchitis (n = 11), and sarcoidosis (n = 9) and from atopic (n = 7) and nonatopic (n = 10) healthy control subjects. Methods Bronchial biopsy specimens were examined for the presence of IL-9 and IL-9R protein and messenger RNA (mRNA) by immunocytochemistry and in situ hybridization, respectively. To phenotype the cells expressing IL-9 in asthmatic tissue, combined in situ hybridization and immunocytochemistry was also performed. Results There was a highly significant difference (P <.001) in the expression of IL-9 mRNA in asthmatic airways (20.6 +/- 4.0 cells/mm of basement membrane) compared with chronic bronchitis (5.6 +/- 4.4), sarcoidosis (2.5 +/- 1.8), atopic control subjects (7.7 +/- 2.2), and healthy control subjects (2.7 +/- 2.3). The number of IL-9 immunoreactive cells was also greater in asthmatic patients compared with the other groups (P <.05). Although the level of IL-9R mRNA expression did not differ in any of the groups (P >.05), IL-9R immunoreactivity was significantly higher in asthmatic compared with control subjects. Furthermore, IL-9 mRNA expression levels were also significantly correlated with FEV(1) (P <.05) and the airway responsiveness to methacholine producing a 20% fall in FEV(1) (P <. 01). The cells expressing IL-9 mRNA in asthmatic tissue were CD3(+) lymphocytes (68%), major basic protein(+) eosinophils (16%), and elastase(+) neutrophils (8%). Conclusion The results of this study demonstrate the potential of IL-9 to be a marker for atopic asthma and furthermore suggest an important role for this cytokine in the pathophysiologic mechanisms of this disease.
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IL-9 expression is increased in lungs of asthmatic patients.
“IL-9 expression is increased in lungs of asthmatic patients20,21”
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 [21]
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- Authors
- Shimbara, A., Christodoulopoulos, P., Soussi-Gounni, A., Olivenstein, R., Nakamura, Y., Levitt, R. C., Nicolaides, N. C., Holroyd, K. J., Tsicopoulos, A., Lafitte, J.-J., Wallaert, B., & Hamid, Q. A.
- Affiliations
- McGill University (CA)
- Inserm (FR)
- ORCID
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2000-01
- Volume
- 105
- Issue
- 1
- Pages
- 108-115
- ISSN
- 0091-6749 (ISSN-L)
- OpenAlex
- W2090021858
- Cited by
- 281
- References
- 38
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 8 · 2023: 3 · 2022: 9 · 2021: 11 · 2020: 12 · 2019: 10 · 2018: 8 · 2017: 14 · 2016: 12 · 2015: 17 · 2014: 7 · 2013: 15 · 2012: 16
- FWCI
- 11.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Keywords
- IL-9, IL-9 receptor, asthma, allergic asthma, chronic bronchitis, sarcoidosis, airway inflammation, eosinophils, neutrophils, CD3+ T cells, airway hyperresponsiveness, methacholine challenge, FEV1, candidate genes, cytokine expression, lung disease biomarkers
- MeSH terms
- Adult, Asthma, Bronchi, Bronchial Diseases, Bronchitis, Chronic Disease, Female, Humans, Hypersensitivity, Male, Reference Values, RNA, Messenger, Sarcoidosis, Interleukin-9, Receptors, Interleukin, Receptors, Interleukin-9
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