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Sphingosine 1-phosphate (S1P) induced interleukin-8 (IL-8) release is mediated by S1P receptor 2 and nuclear factor κB in BEAS-2B cells
The airway epithelium may release pro-inflammatory cytokines and chemokines in the asthmatic airway. Sphingosine 1-phosphate (S1P) is a bioactive lipid, increased in the airways of asthmatics, that may trigger the release of the potent neutrophil chemoattractant Interleukin-8 (IL-8) by epithelial ce...
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Published in: | PloS one 2014-04, Vol.9 (4), p.e95566-e95566 |
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description | The airway epithelium may release pro-inflammatory cytokines and chemokines in the asthmatic airway. Sphingosine 1-phosphate (S1P) is a bioactive lipid, increased in the airways of asthmatics, that may trigger the release of the potent neutrophil chemoattractant Interleukin-8 (IL-8) by epithelial cells. S1P is a ligand for 5 G protein-coupled receptors, S1PR1-5. We wished to explore the mechanisms of S1P induced IL-8 secretion with regard to the receptor(s) and downstream signaling events involved. Our results indicate that S1P induced IL-8 release is mediated by S1PR2 and the transcription factor NF-κB. Since the Epidermal Growth Factor Receptor (EGFR) and reactive oxygen species (ROS) have been implicated in IL-8 release in response to activation of other G protein-coupled receptors, we examined their importance in S1P induced IL-8 release and established that they are not involved. This study reveals S1PR2 and NF-κB as potential therapeutic targets in neutrophilic airway diseases such as severe asthma. |
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Sphingosine 1-phosphate (S1P) is a bioactive lipid, increased in the airways of asthmatics, that may trigger the release of the potent neutrophil chemoattractant Interleukin-8 (IL-8) by epithelial cells. S1P is a ligand for 5 G protein-coupled receptors, S1PR1-5. We wished to explore the mechanisms of S1P induced IL-8 secretion with regard to the receptor(s) and downstream signaling events involved. Our results indicate that S1P induced IL-8 release is mediated by S1PR2 and the transcription factor NF-κB. Since the Epidermal Growth Factor Receptor (EGFR) and reactive oxygen species (ROS) have been implicated in IL-8 release in response to activation of other G protein-coupled receptors, we examined their importance in S1P induced IL-8 release and established that they are not involved. This study reveals S1PR2 and NF-κB as potential therapeutic targets in neutrophilic airway diseases such as severe asthma.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0095566</identifier><identifier>PMID: 24743449</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Asthma ; Biology and Life Sciences ; Cell Line ; Chemokines ; Cytokines ; Downstream effects ; Epidermal growth factor ; Epidermal growth factor receptors ; Epithelial cells ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelium ; G protein-coupled receptors ; Humans ; Inflammation ; Interleukin ; Interleukin 8 ; Interleukin-8 - metabolism ; Kinases ; Laboratories ; Leukocytes (neutrophilic) ; Lysophospholipids - pharmacology ; Medicine and Health Sciences ; Neutrophils ; NF-kappa B - metabolism ; NF-κB protein ; Oxidative stress ; Oxygen ; Pathogenesis ; Penicillin ; Phosphates ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptor, Epidermal Growth Factor - metabolism ; Receptors ; Receptors, Lysosphingolipid - metabolism ; Respiratory tract diseases ; Rodents ; Signaling ; Smooth muscle ; Sphingosine - analogs & derivatives ; Sphingosine - pharmacology ; Sphingosine 1-phosphate</subject><ispartof>PloS one, 2014-04, Vol.9 (4), p.e95566-e95566</ispartof><rights>2014 O’Sullivan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Sphingosine 1-phosphate (S1P) is a bioactive lipid, increased in the airways of asthmatics, that may trigger the release of the potent neutrophil chemoattractant Interleukin-8 (IL-8) by epithelial cells. S1P is a ligand for 5 G protein-coupled receptors, S1PR1-5. We wished to explore the mechanisms of S1P induced IL-8 secretion with regard to the receptor(s) and downstream signaling events involved. Our results indicate that S1P induced IL-8 release is mediated by S1PR2 and the transcription factor NF-κB. Since the Epidermal Growth Factor Receptor (EGFR) and reactive oxygen species (ROS) have been implicated in IL-8 release in response to activation of other G protein-coupled receptors, we examined their importance in S1P induced IL-8 release and established that they are not involved. This study reveals S1PR2 and NF-κB as potential therapeutic targets in neutrophilic airway diseases such as severe asthma.</description><subject>Asthma</subject><subject>Biology and Life Sciences</subject><subject>Cell Line</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Downstream effects</subject><subject>Epidermal growth factor</subject><subject>Epidermal growth factor receptors</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelium</subject><subject>G protein-coupled receptors</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin</subject><subject>Interleukin 8</subject><subject>Interleukin-8 - metabolism</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lysophospholipids - pharmacology</subject><subject>Medicine and Health Sciences</subject><subject>Neutrophils</subject><subject>NF-kappa B - 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drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelium</topic><topic>G protein-coupled receptors</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin</topic><topic>Interleukin 8</topic><topic>Interleukin-8 - metabolism</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lysophospholipids - pharmacology</topic><topic>Medicine and Health Sciences</topic><topic>Neutrophils</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Oxygen</topic><topic>Pathogenesis</topic><topic>Penicillin</topic><topic>Phosphates</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>Receptors</topic><topic>Receptors, Lysosphingolipid - metabolism</topic><topic>Respiratory tract diseases</topic><topic>Rodents</topic><topic>Signaling</topic><topic>Smooth muscle</topic><topic>Sphingosine - analogs & derivatives</topic><topic>Sphingosine - pharmacology</topic><topic>Sphingosine 1-phosphate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>O'Sullivan, Michael J</creatorcontrib><creatorcontrib>Hirota, Nobuaki</creatorcontrib><creatorcontrib>Martin, James G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>PHMC-Proquest健康医学期刊库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>O'Sullivan, Michael J</au><au>Hirota, Nobuaki</au><au>Martin, James G</au><au>Chu, Hong Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sphingosine 1-phosphate (S1P) induced interleukin-8 (IL-8) release is mediated by S1P receptor 2 and nuclear factor κB in BEAS-2B cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-04-17</date><risdate>2014</risdate><volume>9</volume><issue>4</issue><spage>e95566</spage><epage>e95566</epage><pages>e95566-e95566</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The airway epithelium may release pro-inflammatory cytokines and chemokines in the asthmatic airway. Sphingosine 1-phosphate (S1P) is a bioactive lipid, increased in the airways of asthmatics, that may trigger the release of the potent neutrophil chemoattractant Interleukin-8 (IL-8) by epithelial cells. S1P is a ligand for 5 G protein-coupled receptors, S1PR1-5. We wished to explore the mechanisms of S1P induced IL-8 secretion with regard to the receptor(s) and downstream signaling events involved. Our results indicate that S1P induced IL-8 release is mediated by S1PR2 and the transcription factor NF-κB. Since the Epidermal Growth Factor Receptor (EGFR) and reactive oxygen species (ROS) have been implicated in IL-8 release in response to activation of other G protein-coupled receptors, we examined their importance in S1P induced IL-8 release and established that they are not involved. This study reveals S1PR2 and NF-κB as potential therapeutic targets in neutrophilic airway diseases such as severe asthma.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24743449</pmid><doi>10.1371/journal.pone.0095566</doi><oa>free_for_read</oa></addata></record> |
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subjects | Asthma Biology and Life Sciences Cell Line Chemokines Cytokines Downstream effects Epidermal growth factor Epidermal growth factor receptors Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelium G protein-coupled receptors Humans Inflammation Interleukin Interleukin 8 Interleukin-8 - metabolism Kinases Laboratories Leukocytes (neutrophilic) Lysophospholipids - pharmacology Medicine and Health Sciences Neutrophils NF-kappa B - metabolism NF-κB protein Oxidative stress Oxygen Pathogenesis Penicillin Phosphates Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Receptor, Epidermal Growth Factor - metabolism Receptors Receptors, Lysosphingolipid - metabolism Respiratory tract diseases Rodents Signaling Smooth muscle Sphingosine - analogs & derivatives Sphingosine - pharmacology Sphingosine 1-phosphate |
title | Sphingosine 1-phosphate (S1P) induced interleukin-8 (IL-8) release is mediated by S1P receptor 2 and nuclear factor κB in BEAS-2B cells |
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