ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
IL-17F-induced IL-11 release in bronchial epithelial cells via MSK1-CREB pathway.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. 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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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Microbial biomarker development for detection and prognosis of early-stage non-small cell lung cancer.Cancer biomarkers : section A of Disease markers · 2025Review
- Discovery and Characterization of a Novel Series of Chloropyrimidines as Covalent Inhibitors of the Kinase MSK1.ACS medicinal chemistry letters · 2022Article
- IL-17 Cytokines and Chronic Lung Diseases.Cells · 2022Review
- Mucosal acidosis elicits a unique molecular signature in epithelia and intestinal tissue mediated by GPR31-induced CREB phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Design, Synthesis and Biological Evaluation of Arylpyridin-2-yl Guanidine Derivatives and Cyclic Mimetics as Novel MSK1 Inhibitors. An Application in an Asthma Model.Molecules (Basel, Switzerland) · 2021Article
- Interleukin-11 signaling underlies fibrosis, parenchymal dysfunction, and chronic inflammation of the airway.Experimental & molecular medicine · 2020Review
- Mechanical forces induce an asthma gene signature in healthy airway epithelial cells.Scientific reports · 2020Article
- Expression of mRNA IL-17F and sIL-17F in atopic asthma patients.BMC research notes · 2017Article
- Pulmonary microRNA profiles identify involvement of Creb1 and Sec14l3 in bronchial epithelial changes in allergic asthma.Scientific reports · 2017Article
- Role of Aspergillus fumigatus in Triggering Protease-Activated Receptor-2 in Airway Epithelial Cells and Skewing the Cells toward a T-helper 2 Bias.American journal of respiratory cell and molecular biology · 2016Article
- IL-17A mediates a selective gene expression profile in asthmatic human airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2014Article
- Potential involvement of IL-17F in asthma.Journal of immunology research · 2014Review
- The Role of Mitogen-Activated Protein Kinase-Activated Protein Kinases (MAPKAPKs) in Inflammation.Genes · 2013Article
- IL-17 induces type V collagen overexpression and EMT via TGF-β-dependent pathways in obliterative bronchiolitis.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Angiotensin-(1-7) inhibits allergic inflammation, via the MAS1 receptor, through suppression of ERK1/2- and NF-κB-dependent pathways.British journal of pharmacology · 2012Article
- The AGC kinase inhibitor H89 attenuates airway inflammation in mouse models of asthma.PloS one · 2012Article
- IL-17F Induces CCL20 in Bronchial Epithelial Cells.Journal of allergy · 2011Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
IL-17F is involved in asthma, but its biological function and signaling pathway have not been fully elucidated. IL-11 is clearly expressed in the airway of patients with allergic airway diseases such as asthma and plays an important role in airway remodeling and inflammation. Therefore, we investigated the expression of IL-11 by IL-17F in bronchial epithelial cells. Bronchial epithelial cells were cultured in the presence or absence of IL-17F and/or Th2 cytokines (IL-4 and IL-13) or various kinase inhibitors to analyze the expression of IL-11. Next, activation of mitogen- and stress-activated protein kinase (MSK) 1 by IL-17F was investigated. Moreover, the effect of short interfering RNAs (siRNAs) targeting MSK1 and cAMP response element binding protein (CREB) on IL-17F-induced IL-11 expression was investigated. IL-17F induced IL-11 expression, whereas the costimulation with IL-4 and IL-13 augmented this effect even further. MEK inhibitors PD-98059, U0126, and Raf1 kinase inhibitor I, significantly inhibited IL-11 production, whereas overexpression of a Raf1 dominant-negative mutant inhibited its expression. IL-17F clearly phosphorylated MSK1, whereas PD-98059 inhibited the phosphorylation of IL-17F-induced MSK1. Both MSK1 inhibitors Ro-31-8220 and H89 significantly blocked IL-11 expression. Moreover, transfection of the cells with siRNAs targeting MSK1 inhibited activation of CREB, and the siRNAs targeting MSK1 and CREB blocked expression of IL-11. These data suggest that IL-17F may be involved in airway inflammation and remodeling via the induction of IL-11, and RafI-MEK1/2-ERK1/2-MSK1-CREB is identified as a novel signaling pathway participating in this process. Therefore, the IL-17F/IL-11 axis may be a valuable therapeutic target for asthma.
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