ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
The p110δ subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Roles of PI3K pan-inhibitors and PI3K-δ inhibitors in allergic lung inflammation: a systematic review and meta-analysis.Scientific reports · 2020Pooled it
- Study ofInternational journal of molecular sciences · 2026Article
- Inhibition of protease-activated receptor-2 attenuates multi-walled carbon nanotube exacerbation of allergic lung disease in mice.Particle and fibre toxicology · 2025Article
- Senescent B cells regulate CD38 expression via FOXO1 in pneumonia resulting fromLife medicine · 2025Article
- PI3Kγδ inhibition suppresses key disease features in a rat model of asthma.Respiratory research · 2024Article
- Gene knockdown of CCR3 reduces eosinophilic inflammation and the Th2 immune response by inhibiting the PI3K/AKT pathway in allergic rhinitis mice.Scientific reports · 2022Article
- The Roles of Autophagy, Mitophagy, and the Akt/mTOR Pathway in the Pathogenesis of Chronic Rhinosinusitis with Nasal Polyps.Journal of immunology research · 2022Article
- Selective deletion of SHIP-1 in hematopoietic cells in mice leads to severe lung inflammation involving ILC2 cells.Scientific reports · 2021Article
- Structural and Signaling Events DrivingFrontiers in microbiology · 2021Article
- Phosphatidylinositol 3-kinase-δ controls endoplasmic reticulum membrane fluidity and permeability in fungus-induced allergic inflammation in mice.British journal of pharmacology · 2020Article
- Inhibition of PI3Kδ Enhances Poly I:C-Induced Antiviral Responses and Inhibits Replication of Human Metapneumovirus in Murine Lungs and Human Bronchial Epithelial Cells.Frontiers in immunology · 2020Article
- For Better or Worse: The Potential for Dose Limiting the On-Target Toxicity of PI 3-Kinase Inhibitors.Biomolecules · 2019Review
- Defining Bronchial Asthma with Phosphoinositide 3-Kinase Delta Activation: Towards Endotype-Driven Management.International journal of molecular sciences · 2019Review
- Phosphoinositide 3-kinase-delta could be a biomarker for eosinophilic nasal polyps.Scientific reports · 2018Article
- FABP4 regulates eosinophil recruitment and activation in allergic airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Epstein-Barr Virus-induced Gene 2 Mediates Allergen-induced Leukocyte Migration into Airways.American journal of respiratory and critical care medicine · 2017Article
- Phosphoinositide 3-Kinase in Asthma: Novel Roles and Therapeutic Approaches.American journal of respiratory cell and molecular biology · 2017Review
- Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Phosphoinositide 3-kinase-δ regulates fungus-induced allergic lung inflammation through endoplasmic reticulum stress.Thorax · 2016Article
- Endothelial and leukocyte heparan sulfates regulate the development of allergen-induced airway remodeling in a mouse model.Glycobiology · 2014Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Trafficking and recruitment of eosinophils during allergic airway inflammation is mediated by the phosphatidylinositol 3-kinase (PI3K) family of signaling molecules. The role played by the p110δ subunit of PI3K (PI3K p110δ) in regulating eosinophil trafficking and recruitment was investigated using a selective pharmacological inhibitor (IC87114). Treatment with the PI3K p110δ inhibitor significantly reduced murine bone marrow-derived eosinophil (BM-Eos) adhesion to VCAM-1 as well as ICAM-1 and inhibited activation-induced changes in cell morphology associated with reduced Mac-1 expression and aberrant cell surface localization/distribution of Mac-1 and α4. Infused BM-Eos demonstrated significantly decreased rolling and adhesion in inflamed cremaster muscle microvessels of mice treated with IC87114 compared with vehicle-treated mice. Furthermore, inhibition of PI3K p110δ significantly attenuated eotaxin-1-induced BM-Eos migration and prevented eotaxin-1-induced changes in the cytoskeleton and cell morphology. Knockdown of PI3K p110δ with siRNA in BM-Eos resulted in reduced rolling, adhesion, and migration, as well as inhibition of activation-induced changes in cell morphology, validating its role in regulating trafficking and migration. Finally, in a mouse model of cockroach antigen-induced allergic airway inflammation, oral administration of the PI3K p110δ inhibitor significantly inhibited airway eosinophil recruitment, resulting in attenuation of airway hyperresponsiveness in response to methacholine, reduced mucus secretion, and expression of proinflammatory molecules (found in inflammatory zone-1 and intelectin-1). Overall, these findings indicate the important role played by PI3K p110δ in mediating BM-Eos trafficking and migration by regulating adhesion molecule expression and localization/distribution as well as promoting changes in cell morphology that favor recruitment during inflammation.
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