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<publisher>HAL CCSD</publisher>
<title lang=en>AhR and Arnt differentially regulate NF-κB signaling and chemokine responses in human bronchial epithelial cells.</title>
<creator>Øvrevik, Johan</creator>
<creator>Låg, Marit</creator>
<creator>Lecureur, Valerie</creator>
<creator>Gilot, David</creator>
<creator>Lagadic-Gossmann, Dominique</creator>
<creator>Refsnes, Magne</creator>
<creator>Schwarze, Per , </creator>
<creator>Skuland, Tonje</creator>
<creator>Becher, Rune</creator>
<creator>Holme, Jørn , </creator>
<contributor>Division of Environmental Medicine ; Norwegian Institute of Public Health</contributor>
<contributor>Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC) ; Université de Rennes 1 (UR1) - IFR140</contributor>
<contributor>Contaminants Chimiques, immunité et Inflammation ; Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Institut de Génétique et Développement de Rennes (IGDR) ; Université de Rennes 1 (UR1) - Centre National de la Recherche Scientifique (CNRS) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>The work was supported by the ResearchCouncil of Norway, through the Environmental Exposures and HealthOutcomes-program (MILPAAHEL; grants no. 185620 and 228143).</contributor>
<description>International audience</description>
<source>ISSN: 1478-811X</source>
<source>Cell Communication and Signaling</source>
<publisher>BioMed Central</publisher>
<identifier>inserm-01085082</identifier>
<identifier>http://www.hal.inserm.fr/inserm-01085082</identifier>
<identifier>http://www.hal.inserm.fr/inserm-01085082/document</identifier>
<identifier>http://www.hal.inserm.fr/inserm-01085082/file/s12964-014-0048-8.pdf</identifier>
<source>http://www.hal.inserm.fr/inserm-01085082</source>
<source>Cell Communication and Signaling, BioMed Central, 2013, 12, pp.48. 〈10.1186/s12964-014-0048-8〉</source>
<identifier>PUBMED : 25201625</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/25201625</relation>
<identifier>DOI : 10.1186/s12964-014-0048-8</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1186/s12964-014-0048-8</relation>
<language>en</language>
<subject lang=en>Lung epithelial cells</subject>
<subject lang=en>Inflammation</subject>
<subject lang=en>RelB</subject>
<subject lang=en>p65</subject>
<subject lang=en>Nuclear factor NF- κ B</subject>
<subject lang=en>RANTES</subject>
<subject lang=en>interleukin-8</subject>
<subject lang=en>AhR nuclear translocator</subject>
<subject lang=en>Aryl hydrocarbon receptor</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<subject>[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>BACKGROUND: The aryl hydrocarbon receptor (AhR) has gradually emerged as a regulator of inflammation in the lung and other tissues. AhR may interact with the p65-subunit of the nuclear factor (NF)-κB transcription factors, but reported outcomes of AhR/NF-κB-interactions are conflicting. Some studies suggest that AhR possess pro-inflammatory activities while others suggest that AhR may be anti-inflammatory. The present study explored the impact of AhR and its binding partner AhR nuclear translocator (Arnt) on p65-activation and two differentially regulated chemokines, CXCL8 (IL-8) and CCL5 (RANTES), in human bronchial epithelial cells (BEAS-2B). RESULTS: Cells were exposed to CXCL8- and CCL5-inducing chemicals, 1-nitropyrene (1-NP) and 1-aminopyrene (1-AP) respectively, or the synthetic double-stranded RNA analogue, polyinosinic-polycytidylic acid (Poly I:C) which induced both chemokines. Only CXCL8, and not CCL5, appeared to be p65-dependent. Yet, constitutively active unligated AhR suppressed both CXCL8 and CCL5, as shown by siRNA knock-down and the AhR antagonist α-naphthoflavone. Moreover, AhR suppressed activation of p65 by TNF-α and Poly I:C as assessed by luciferase-assay and p65-phosphorylation at serine 536, without affecting basal p65-activity. In contrast, Arnt suppressed only CXCL8, but did not prevent the p65-activation directly. However, Arnt suppressed expression of the NF-κB-subunit RelB which is under transcriptional regulation by p65. Furthermore, AhR-ligands alone at high concentrations induced a moderate CXCL8-response, without affecting CCL5, but suppressed both CXCL8 and CCL5-responses by Poly I:C. CONCLUSION: AhR and Arnt may differentially and independently regulate chemokine-responses induced by both inhaled pollutants and pulmonary infections. Constitutively active, unligated AhR suppressed the activation of p65, while Arnt may possibly interfere with the action of activated p65. Moreover, ligand-activated AhR suppressed CXCL8 and CCL5 responses by other agents, but AhR ligands alone induced CXCL8 responses when given at sufficiently high concentrations, thus underscoring the duality of AhR in regulation of inflammation. We propose that AhR-signaling may be a weak activator of p65-signaling that suppresses p65-activity induced by strong activators of NF-κB, but that its anti-inflammatory properties also are due to interference with additional pathways.</description>
<date>2013-11-30</date>
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