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Transforming Growth Factor-β and Interleukin-1β Signaling Pathways Converge on the Chemokine CCL20 Promoter

CCL20 is the only chemokine ligand for the chemokine receptor CCR6, which is expressed by the critical antigen presenting cells, dendritic cells. Increased expression of CCL20 is likely involved in the increased recruitment of dendritic cells observed in fibroinflammatory diseases such as chronic ob...

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Published in:The Journal of biological chemistry 2015-06, Vol.290 (23), p.14717-14728
Main Authors: Brand, Oliver J., Somanath, Sangeeta, Moermans, Catherine, Yanagisawa, Haruhiko, Hashimoto, Mitsuo, Cambier, Stephanie, Markovics, Jennifer, Bondesson, Andrew J., Hill, Arthur, Jablons, David, Wolters, Paul, Lou, Jianlong, Marks, James D., Baron, Jody L., Nishimura, Stephen L.
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cited_by cdi_FETCH-LOGICAL-c443t-8b9b0f3bf8d83f6af3bf944fdb64bc577136e97733eb3b7a0de250342298de413
cites cdi_FETCH-LOGICAL-c443t-8b9b0f3bf8d83f6af3bf944fdb64bc577136e97733eb3b7a0de250342298de413
container_end_page 14728
container_issue 23
container_start_page 14717
container_title The Journal of biological chemistry
container_volume 290
creator Brand, Oliver J.
Somanath, Sangeeta
Moermans, Catherine
Yanagisawa, Haruhiko
Hashimoto, Mitsuo
Cambier, Stephanie
Markovics, Jennifer
Bondesson, Andrew J.
Hill, Arthur
Jablons, David
Wolters, Paul
Lou, Jianlong
Marks, James D.
Baron, Jody L.
Nishimura, Stephen L.
description CCL20 is the only chemokine ligand for the chemokine receptor CCR6, which is expressed by the critical antigen presenting cells, dendritic cells. Increased expression of CCL20 is likely involved in the increased recruitment of dendritic cells observed in fibroinflammatory diseases such as chronic obstructive pulmonary disease (COPD). CCL20 expression is increased by the proinflammatory cytokine IL-1β. We have determined that IL-1β-dependent CCL20 expression is also dependent on the multifunctional cytokine TGF-β. TGF-β is expressed in a latent form that must be activated to function, and activation is achieved through binding to the integrin αvβ8 (itgb8). Here we confirm correlative increases in αvβ8 and IL-1β with CCL20 protein in lung parenchymal lysates of a large cohort of COPD patients. How IL-1β- and αvβ8-mediated TGF-β activation conspire to increase fibroblast CCL20 expression remains unknown, because these pathways have not been shown to directly interact. We evaluate the 5′-flanking region of CCL20 to determine that IL-1β-driven CCL20 expression is dependent on αvβ8-mediated activation of TGF-β. We identify a TGF-β-responsive element (i.e. SMAD) located on an upstream enhancer of the human CCL20 promoter required for efficient IL-1β-dependent CCL20 expression. By chromatin immunoprecipitation, this upstream enhancer complexes with the p50 subunit of NF-κB on a NF-κB-binding element close to the transcriptional start site of CCL20. These interactions are confirmed by electromobility shift assays in nuclear extracts from human lung fibroblasts. These data define a mechanism by which αvβ8-dependent activation of TGF-β regulates IL-1β-dependent CCL20 expression in COPD. Background: Mechanisms that drive chronic inflammation in airway disease are not well understood. Results: We demonstrate a TGF-β-responsive enhancer element required for efficient IL-1β-dependent expression of the proinflammatory chemokine CCL20 by human lung fibroblasts. Conclusion: Convergence of TGF-β and IL-1β signaling pathways on the CCL20 promoter are required for efficient fibroblast expression of CCL20. Significance: These findings identify potential targets to reduce chronic inflammation in airway disease.
doi_str_mv 10.1074/jbc.M114.630368
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Increased expression of CCL20 is likely involved in the increased recruitment of dendritic cells observed in fibroinflammatory diseases such as chronic obstructive pulmonary disease (COPD). CCL20 expression is increased by the proinflammatory cytokine IL-1β. We have determined that IL-1β-dependent CCL20 expression is also dependent on the multifunctional cytokine TGF-β. TGF-β is expressed in a latent form that must be activated to function, and activation is achieved through binding to the integrin αvβ8 (itgb8). Here we confirm correlative increases in αvβ8 and IL-1β with CCL20 protein in lung parenchymal lysates of a large cohort of COPD patients. How IL-1β- and αvβ8-mediated TGF-β activation conspire to increase fibroblast CCL20 expression remains unknown, because these pathways have not been shown to directly interact. We evaluate the 5′-flanking region of CCL20 to determine that IL-1β-driven CCL20 expression is dependent on αvβ8-mediated activation of TGF-β. We identify a TGF-β-responsive element (i.e. SMAD) located on an upstream enhancer of the human CCL20 promoter required for efficient IL-1β-dependent CCL20 expression. By chromatin immunoprecipitation, this upstream enhancer complexes with the p50 subunit of NF-κB on a NF-κB-binding element close to the transcriptional start site of CCL20. These interactions are confirmed by electromobility shift assays in nuclear extracts from human lung fibroblasts. These data define a mechanism by which αvβ8-dependent activation of TGF-β regulates IL-1β-dependent CCL20 expression in COPD. Background: Mechanisms that drive chronic inflammation in airway disease are not well understood. Results: We demonstrate a TGF-β-responsive enhancer element required for efficient IL-1β-dependent expression of the proinflammatory chemokine CCL20 by human lung fibroblasts. Conclusion: Convergence of TGF-β and IL-1β signaling pathways on the CCL20 promoter are required for efficient fibroblast expression of CCL20. 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Increased expression of CCL20 is likely involved in the increased recruitment of dendritic cells observed in fibroinflammatory diseases such as chronic obstructive pulmonary disease (COPD). CCL20 expression is increased by the proinflammatory cytokine IL-1β. We have determined that IL-1β-dependent CCL20 expression is also dependent on the multifunctional cytokine TGF-β. TGF-β is expressed in a latent form that must be activated to function, and activation is achieved through binding to the integrin αvβ8 (itgb8). Here we confirm correlative increases in αvβ8 and IL-1β with CCL20 protein in lung parenchymal lysates of a large cohort of COPD patients. How IL-1β- and αvβ8-mediated TGF-β activation conspire to increase fibroblast CCL20 expression remains unknown, because these pathways have not been shown to directly interact. We evaluate the 5′-flanking region of CCL20 to determine that IL-1β-driven CCL20 expression is dependent on αvβ8-mediated activation of TGF-β. We identify a TGF-β-responsive element (i.e. SMAD) located on an upstream enhancer of the human CCL20 promoter required for efficient IL-1β-dependent CCL20 expression. By chromatin immunoprecipitation, this upstream enhancer complexes with the p50 subunit of NF-κB on a NF-κB-binding element close to the transcriptional start site of CCL20. These interactions are confirmed by electromobility shift assays in nuclear extracts from human lung fibroblasts. These data define a mechanism by which αvβ8-dependent activation of TGF-β regulates IL-1β-dependent CCL20 expression in COPD. Background: Mechanisms that drive chronic inflammation in airway disease are not well understood. Results: We demonstrate a TGF-β-responsive enhancer element required for efficient IL-1β-dependent expression of the proinflammatory chemokine CCL20 by human lung fibroblasts. Conclusion: Convergence of TGF-β and IL-1β signaling pathways on the CCL20 promoter are required for efficient fibroblast expression of CCL20. Significance: These findings identify potential targets to reduce chronic inflammation in airway disease.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25918170</pmid><doi>10.1074/jbc.M114.630368</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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ispartof The Journal of biological chemistry, 2015-06, Vol.290 (23), p.14717-14728
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source ScienceDirect®; PubMed Central
subjects Animals
Base Sequence
Cells, Cultured
chemokine
Chemokine CCL20 - genetics
Fibroblasts - immunology
Fibroblasts - metabolism
Gene Expression Regulation
Humans
inflammation
integrin
Interleukin-1beta - immunology
Lung - cytology
Mice
Mice, Inbred C57BL
Molecular Bases of Disease
NF-kappa B - immunology
Response Elements
Signal Transduction
TGF-β
transcription
Transforming Growth Factor beta - immunology
title Transforming Growth Factor-β and Interleukin-1β Signaling Pathways Converge on the Chemokine CCL20 Promoter
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