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Cited by 142Asthma and respiratory diseasesIL-33, ST2, and ILC PathwaysAllergic Rhinitis and Sensitization

The Absence of Interleukin 9 Does Not Affect the Development of Allergen-induced Pulmonary Inflammation nor Airway Hyperreactivity

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McMillan, Sarah J., Bishop, Benjamin, Townsend, Michael J., McKenzie, Andrew N., Lloyd, Clare M.·2002·The Journal of Experimental Medicine
DOI 10.1084/jem.20011732PMC PMC2196020
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Abstract

Interleukin (IL)-9 is a pleiotropic cytokine secreted by T helper (Th)2 cells and has been proposed as a candidate gene for asthma and allergy. We have used mice genetically deficient in IL-9 to determine the role of this cytokine in the pathophysiologic features of the allergic pulmonary response–airway hyperreactivity (AHR) and eosinophilia. We have demonstrated that IL-9 is not required for the development of a robust Th2 response to allergen in sensitized mice. IL-9 knockout mice developed a similar degree of eosinophilic inflammation and AHR to their wild-type littermates. Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9. Moreover, levels of bronchoalveolar lavage (BAL) IL-4, IL-5, and IL-13 were comparable between wild-type and knockout mice. These findings indicate that IL-9 is not obligatory for the development of eosinophilia and AHR, and imply that other Th2 cytokines can act in a compensatory fashion.

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  • Blockade of IL-9 in a standard sensitization-challenge model results in decreased allergic inflammation.

    “blockade of IL-9 in a similar model results in decreased allergic inflammation18,19.”

    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 [19]

    In Results and Discussion, under “Development of Pulmonary Inflammation in the Absence of IL-9” (page unavailable), the paper reports comparable inflammatory-cell recruitment in allergen-challenged IL-9–deficient and wild-type mice, not decreased inflammation. It studied genetic IL-9 deficiency rather than pharmacological blockade. (LLM, conf=0.88)

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Authors
McMillan, S. J., Bishop, B., Townsend, M. J., McKenzie, A. N., & Lloyd, C. M.
Affiliations
  • Imperial College London (GB)
  • MRC Laboratory of Molecular Biology (GB)
ORCID
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2002-01-07
Volume
195
Issue
1
Pages
51-57
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.20011732
PMC
PMC2196020
OpenAlex
W2163544819
Cited by
142
References
2
Citations by year
2026: 1 · 2025: 4 · 2024: 3 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 5 · 2018: 3 · 2017: 6 · 2016: 6 · 2015: 4 · 2014: 1 · 2013: 7 · 2012: 7
FWCI
8.41
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
Wellcome Trust (087618, 057704)
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, allergic airway inflammation, airway hyperresponsiveness, eosinophilia, Th2 cells, Th2 cytokines, goblet cell hyperplasia, IgE, IL-4, IL-5, IL-13, asthma, allergy
MeSH terms
Animals, Bronchoalveolar Lavage Fluid, Cell Count, Eosinophilia, Hyperplasia, Immunoglobulin E, Interleukins, Mice, Mutant Strains, Mucus, Pneumonia, Respiratory Hypersensitivity, Interleukin-9, Th2 Cells, Chemokines, CC, Goblet Cells, Mice, Chemokine CCL11

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