| Regulation and function of the IL-1 family cytokine IL-1F9 in human bronchial epithelial cells. | |
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MedLine Citation:
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PMID: 20870894 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The IL-1 family of cytokines, which now includes 11 members, is well known to participate in inflammation. Although the most recently recognized IL-1 family cytokines (IL-1F5-11) have been shown to be expressed in airway epithelial cells, the regulation of their expression and function in the epithelium has not been extensively studied. We investigated the regulation of IL-1F5-11 in primary normal human bronchial epithelial cells. Messenger (m)RNAs for IL-1F6 and IL-1F9, but not IL-1F5, IL-1F8 or IL-1F10, were significantly up-regulated by TNF, IL-1β, IL-17 and the Toll-like receptor (TLR)3 ligand double-stranded (ds)RNA. mRNAs for IL-1F7 and IL-1F11 (IL-33) were weakly up-regulated by some of the cytokines tested. Notably, mRNAs for IL-1F6 and IL-1F9 were synergistically enhanced by the combination of TNF/IL-17 or dsRNA/IL-17. IL-1F9 protein was detected in the supernatant following stimulation with dsRNA or a combination of dsRNA and IL-17. IL-1F6 protein was detected in the cell lysate but was not detected in the supernatant. We screened for the receptor for IL-1F9 and found that lung fibroblasts expressed this receptor. We found that IL-1F9 activated mitogen-activated protein kinases and the transcription factor NF-κB in primary normal human lung fibroblasts. IL-1F9 also stimulated the expression of the neutrophil chemokines IL-8 and CXCL3 and the Th17 chemokine CCL20 in lung fibroblasts. These results suggest that epithelial activation by TLR3 (e.g., by respiratory viral infection) and exposure to cytokines from Th17 cells (IL-17) and inflammatory cells (TNF) may amplify neutrophilic inflammation in the airway via induction of IL-1F9 and activation of fibroblasts. |
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Authors:
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Regina T Chustz; Deepti R Nagarkar; Julie A Poposki; Silvio Favoreto; Pedro C Avila; Robert P Schleimer; Atsushi Kato |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-09-24 |
Journal Detail:
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Title: American journal of respiratory cell and molecular biology Volume: 45 ISSN: 1535-4989 ISO Abbreviation: Am. J. Respir. Cell Mol. Biol. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-07-13 Completed Date: 2011-09-08 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 8917225 Medline TA: Am J Respir Cell Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 145-53 Citation Subset: IM |
Affiliation:
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Division of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, 240 E. Huron, Chicago, IL 60611, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Bronchi
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cytology,
metabolism* Cytokines / metabolism Epithelial Cells / cytology, metabolism* Fibroblasts / cytology, metabolism Humans Inflammation / metabolism Interleukin-1 / biosynthesis* Lung / cytology, metabolism Mitogen-Activated Protein Kinase Kinases / metabolism NF-kappa B / metabolism RNA, Double-Stranded / pharmacology RNA, Messenger / biosynthesis Respiratory Mucosa / cytology, metabolism* Toll-Like Receptor 3 / metabolism Up-Regulation / drug effects, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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R01 AI072570-03/AI/NIAID NIH HHS; R01 AI072570-05/AI/NIAID NIH HHS; R01 HL068546-25/HL/NHLBI NIH HHS; R01 HL078860-05A1/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/IL36G protein, human; 0/Interleukin-1; 0/NF-kappa B; 0/RNA, Double-Stranded; 0/RNA, Messenger; 0/TLR3 protein, human; 0/Toll-Like Receptor 3; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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