ArticleMediators of inflammation2019
Epigenetic Regulation of IL-17-Induced Chemokines in Lung Epithelial Cells.
Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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
15 citing papers in PubMed, 23 citations in OpenAlex.
- Epigenetic regulation and chromatin organization in cystic fibrosis airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Review
- IL-1 family signalling drives mucosal defence against systemic Candida albicans infection.Nature microbiology · 2026Article
- Pediatric bronchial ulcers induced by ibuprofen overdose: a case report combined with network toxicology to decipher potential mechanisms.Frontiers in pharmacology · 2026Article
- Advances in understanding the role of interleukins in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2025Review
- Weighted Breaths: Exploring Biologic and Non-Biologic Therapies for Co-Existing Asthma and Obesity.Current allergy and asthma reports · 2024Review
- Asthma-associated bacterial infections: Are they protective or deleterious?The journal of allergy and clinical immunology. Global · 2023Review
- Dynamic Changes of NCRInflammation · 2022Article
- Molecular Mechanism of Biofilm Locator Protein Kinase Dbf2p-related kinase 1 in Regulating Innate Immune Response to Interleukin 17-induced Viral Pneumonia.Bioengineered · 2021Article
- C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial-mesenchymal transition in COPD mice.BMC pulmonary medicine · 2021Article
- Role of Epigenetics in the Regulation of Immune Functions of the Skin.The Journal of investigative dermatology · 2021Review
- Bronchial epithelial DNA methyltransferase 3b dampens pulmonary immune responses during Pseudomonas aeruginosa infection.PLoS pathogens · 2021Article
- Regulation of Immune Responses by Nonhematopoietic Cells in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Bronchial Epithelial Tet2 Maintains Epithelial Integrity during Acute Pseudomonas aeruginosa Pneumonia.Infection and immunity · 2020Article
- The role of interleukin-17 in asthma: a protective response?ERJ open research · 2020Review
- Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling.BMC pulmonary medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Epithelial cells are known to have barrier functions in multiple organs and regulate innate immune responses. Airway epithelial cells respond to IL-17 by altering their transcriptional profiles and producing antimicrobial proteins and neutrophil chemoattractants. Although IL-17 has been shown to promote inflammation through stabilizing mRNA of CXCR2 ligands, how IL-17 exerts its downstream effects on its target cells through epigenetic mechanisms is largely unknown. Using primary human bronchial epithelial cells and immortalized epithelial cell line from both human and mouse, we demonstrated that IL-17-induced CXCR2 ligand production is dependent on histone acetylation specifically through repressing HDAC5. Furthermore, the chemokine production induced by IL-17 is strictly dependent on the bromodomain and extraterminal domain (BET) family as BET inhibition abolished the IL-17A-induced proinflammatory chemokine production, indicating a pivotal role of the recognition of acetylated histones. In combination with single-cell RNA-seq analysis, we revealed that the cell lines we employed represent specific lineages and their IL-17 responses were regulated differently by the DNA methylation mechanisms. Taken together, our data strongly support that IL-17 sustains epithelial CXCR2 ligand production through epigenetic regulation and the therapeutic potential of interrupting histone modification as well as the recognition of modified histones could be evaluated in neutrophilic lung diseases.
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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.