ArticlePloS one2018
IL-13 induces periostin and eotaxin expression in human primary alveolar epithelial cells: Comparison with paired airway epithelial cells.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Effect of Dupilumab on Type 2 Biomarkers in Chronic Rhinosinusitis With Nasal Polyps: SINUS-52 Study Results.The Annals of otology, rhinology, and laryngology · 2023Trial
- The involvement of Th17 inflammation and miR-363-3p in airway epithelial barrier dysfunction.Respiratory research · 2026Article
- Cellular and molecular features of asthma mucus plugs provide clues about their formation and persistence.The Journal of clinical investigation · 2025Article
- Emerging Concepts in Cytokine Regulation of Airway Remodeling in Asthma.Immunological reviews · 2025Review
- Exploring the pathogenesis and clinical implications of asthma, chronic obstructive pulmonary disease (COPD), and asthma-COPD overlap (ACO): a narrative review.Frontiers in medicine · 2025Review
- Cell-Specific Contribution of IL-4 Receptor α Signaling Shapes the Overall Manifestation of Allergic Airway Disease.American journal of respiratory cell and molecular biology · 2024Article
- Integrative Cross-Talk in Asthma: Unraveling the Complex Interactions Between Eosinophils, Immune, and Structural Cells in the Airway Microenvironment.Diagnostics (Basel, Switzerland) · 2024Review
- Inflammatory Cytokine Elaboration Following Secondhand Smoke (SHS) Exposure Is Mediated in Part by RAGE Signaling.International journal of molecular sciences · 2023Article
- Article
- Destructive fibrotic teamwork: how both microenvironment stiffness and profibrotic interleukin 13 impair alveolar macrophage phenotype and function.Biomaterials science · 2022Article
- Viral infection and allergy status impact severity of asthma symptoms in children with asthma exacerbations.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022Article
- Elevated serum periostin levels among arsenic-exposed individuals and their associations with the features of asthma.Chemosphere · 2022Article
- The Airway Epithelium-A Central Player in Asthma Pathogenesis.International journal of molecular sciences · 2020Review
- Interleukin-13 disrupts type 2 pneumocyte stem cell activity.JCI insight · 2020Article
- Apolipoprotein E and Periostin Are Potential Biomarkers of Nasal Mucosal Inflammation. A Parallel Approach ofAmerican journal of respiratory cell and molecular biology · 2020Article
- Which Factors Associated With Activated Eosinophils Contribute to the Pathogenesis of Aspirin-Exacerbated Respiratory Disease?Allergy, asthma & immunology research · 2019Review
- The effect of BPIFA1/SPLUNC1 genetic variation on its expression and function in asthmatic airway epithelium.JCI insight · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar epithelial cells are critical to the pathogenesis of pulmonary inflammation and fibrosis, which are associated with overexpression of type 2 cytokine IL-13. IL-13 is known to induce the production of profibrotic (e.g., periostin) and pro-inflammatory (e.g., eotaxin-3) mediators in human airway epithelial cells, but it remains unclear if human primary alveolar epithelial cells increase periostin and eotaxin expression following IL-13 stimulation. The goals of this study are to determine if alveolar epithelial cells increase periostin and eotaxin expression upon IL-13 stimulation, and if alveolar and airway epithelial cells from the same subjects have similar responses to IL-13. Paired alveolar and airway epithelial cells were isolated from donors without any lung disease, and cultured under submerged or air-liquid interface conditions with or without IL-13. Up-regulation of periostin protein and mRNA was observed in IL-13-stimulated alveolar epithelial cells, which was comparable to that in IL-13-stimulated paired airway epithelial cells. IL-13 also increased eotaxin-3 expression in alveolar epithelial cells, but the level of eotaxin mRNA was lower in alveolar epithelial cells than in airway epithelial cells. Our findings demonstrate that human alveolar epithelial cells are able to produce periostin and eotaxin in responses to IL-13 stimulation. This study suggests the need to further determine the contribution of alveolar epithelial cell-derived mediators to pulmonary fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.