ArticleRespiratory research2005
Airway allergen exposure stimulates bone marrow eosinophilia partly via IL-9.
Article in Respiratory research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 36 citations in OpenAlex.
- The Pleiotropic IL-9 Network in Asthma Pathogenesis and Targeted Therapy.Journal of inflammation research · 2026Review
- Pathobiology and Regulation of Eosinophils, Mast Cells, and Basophils in Allergic Asthma.Immunological reviews · 2025Review
- Increased allergic inflammation and decreased lung insulin sensitivity in offspring of obese allergic mothers.Journal of leukocyte biology · 2024Article
- The World according to IL-9.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Odd couple: The unexpected partnership of glucocorticoid hormones and cysteinyl-leukotrienes in the extrinsic regulation of murine bone-marrow eosinopoiesis.World journal of experimental medicine · 2017Review
- Th9 cells in the pathogenesis of EAE and multiple sclerosis.Seminars in immunopathology · 2017Review
- Pathogenesis of eosinophilic chronic rhinosinusitis.Journal of inflammation (London, England) · 2016Review
- Allergenicity and toxicology of inhaled silver nanoparticles in allergen-provocation mice models.International journal of nanomedicine · 2013Article
- Cellular sources and immune functions of interleukin-9.Nature reviews. Immunology · 2010Review
- New drugs targeting Th2 lymphocytes in asthma.Journal of occupational medicine and toxicology (London, England) · 2008Article
- Regulatory role of CD8+ T lymphocytes in bone marrow eosinophilopoiesis.Respiratory research · 2006Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin (IL)-9 is a Th2-derived cytokine with pleiotropic biological effects, which recently has been proposed as a candidate gene for asthma and allergy. We aimed to evaluate the therapeutic effect of a neutralizing anti-IL-9 antibody in a mouse model of airway eosinophilic inflammation and compared any such effect with anti-IL-5 treatment.
methodsOVA-sensitized Balb/c mice were intraperitoneally pretreated with a single dose (100 microg) of an anti-mouse IL-9 monoclonal antibody (clone D9302C12) or its vehicle. A third group was given 50 microg of a monoclonal anti-mouse IL-5 antibody (TRFK-5) or its vehicle. Animals were subsequently exposed to OVA on five days via airways. Newly produced eosinophils were labelled using 5-bromo-2'-deoxyuridine (BrdU). BrdU+ eosinophils and CD34+ cell numbers were examined by immunocytochemistry. After culture and stimulation with OVA or PMA+IC, intracellular staining of IL-9 in bone marrow cells from OVA-exposed animals was measured by Flow Cytometry. The Mann-Whitney U-test was used to determine significant differences between groups.
resultsAnti-IL-9 significantly reduced bone marrow eosinophilia, primarily by decrease of newly produced (BrdU+) and mature eosinophils. Anti-IL-9 treatment also reduced blood neutrophil counts, but did not affect BAL neutrophils. Anti-IL-5 was able to reduce eosinophil numbers in all tissue compartments, as well as BrdU+ eosinophils and CD34+ progenitor cells, and in all instances to a greater extent than anti-IL-9. Also, FACS analysis showed that IL-9 is over-expressed in bone marrow CD4+ cells after allergen exposure.
conclusionsOur data shows that a single dose of a neutralizing IL-9 antibody is not sufficient to reduce allergen-induced influx of newly produced cells from bone marrow to airways. However, in response to allergen, bone marrow cells over-express IL-9. This data suggest that IL-9 may participate in the regulation of granulocytopoiesis in allergic inflammation.
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