Effect of Th1/Th2 Cytokine Pretreatment on RSV-Induced Gene Expression in Airway Epithelial Cells
Background: Respiratory syncytial virus (RSV) infection in infants with Th2 predisposition is thought to increase the risk of allergic sensitization, recurrent wheezing, and bronchial asthma during childhood. We attempted to clarify the molecular mechanisms by which Th1/Th2 predisposition in the hos...
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| Veröffentlicht in: | International archives of allergy and immunology 2011-01, Vol.154 (3), p.185-194 |
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| creator | Yamada, Yumi Matsumoto, Kenji Hashimoto, Noriko Saikusa, Miwako Homma, Toshiki Yoshihara, Shigemi Saito, Hirohisa |
| description | Background: Respiratory syncytial virus (RSV) infection in infants with Th2 predisposition is thought to increase the risk of allergic sensitization, recurrent wheezing, and bronchial asthma during childhood. We attempted to clarify the molecular mechanisms by which Th1/Th2 predisposition in the host alters RSV infection and facilitates airway inflammation. Methods: A549 human airway epithelial cells were inoculated with live or UV-treated RSV after pretreatment with either a combination of tumor necrosis factor (TNF)-α and interferon-γ (Th1-primed) or a combination of TNF-α and interleukin-4 (Th2-primed) for 48 h. The gene and protein expression profiles of RSV-infected A549 cells were examined. Results: GeneChip analysis indicated that, at 96 h after inoculation with RSV, the expression of 62 genes was specifically enhanced (more than 2-fold by normalized data) in Th2-primed cells compared to that in unprimed or Th1-primed cells. An increase in mRNA and protein levels of monocyte chemoattractant protein (MCP)-1/CCL2 among those 62 genes was confirmed by real-time PCR and cytometric bead assay, respectively. RSV replication was markedly diminished in Th1-primed airway epithelial cells but not in Th2-primed cells, which was presumably caused at least in part by the early induction of antiviral genes. Conclusions: These results suggest that Th1/Th2 predisposition in the host prior to RSV infection critically regulates inflammatory reactions in the airways through alteration of gene expression, and that MCP-1/CCL2 plays an important role in the pathogenesis of severe RSV infection and the subsequent development of asthma in Th2-predisposed hosts. |
| doi_str_mv | 10.1159/000321105 |
| format | Article |
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We attempted to clarify the molecular mechanisms by which Th1/Th2 predisposition in the host alters RSV infection and facilitates airway inflammation. Methods: A549 human airway epithelial cells were inoculated with live or UV-treated RSV after pretreatment with either a combination of tumor necrosis factor (TNF)-α and interferon-γ (Th1-primed) or a combination of TNF-α and interleukin-4 (Th2-primed) for 48 h. The gene and protein expression profiles of RSV-infected A549 cells were examined. Results: GeneChip analysis indicated that, at 96 h after inoculation with RSV, the expression of 62 genes was specifically enhanced (more than 2-fold by normalized data) in Th2-primed cells compared to that in unprimed or Th1-primed cells. An increase in mRNA and protein levels of monocyte chemoattractant protein (MCP)-1/CCL2 among those 62 genes was confirmed by real-time PCR and cytometric bead assay, respectively. RSV replication was markedly diminished in Th1-primed airway epithelial cells but not in Th2-primed cells, which was presumably caused at least in part by the early induction of antiviral genes. Conclusions: These results suggest that Th1/Th2 predisposition in the host prior to RSV infection critically regulates inflammatory reactions in the airways through alteration of gene expression, and that MCP-1/CCL2 plays an important role in the pathogenesis of severe RSV infection and the subsequent development of asthma in Th2-predisposed hosts.</description><identifier>ISSN: 1018-2438</identifier><identifier>EISSN: 1423-0097</identifier><identifier>DOI: 10.1159/000321105</identifier><identifier>PMID: 20861640</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Asthma ; Babies ; Biological and medical sciences ; Cell Line ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Cytokines - genetics ; Cytokines - metabolism ; Epithelial Cells - drug effects ; Epithelial Cells - immunology ; Epithelial Cells - metabolism ; Epithelial Cells - virology ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Gene Expression Profiling ; Gene Expression Regulation ; Human viral diseases ; Humans ; Immunopathology ; Infectious diseases ; Interferon-gamma - metabolism ; Interferon-gamma - pharmacology ; Lung - cytology ; Lung - drug effects ; Lung - immunology ; Lung - metabolism ; Lung - virology ; Medical sciences ; Oligonucleotide Array Sequence Analysis ; Original Paper ; Pathogenesis ; Respiratory syncytial virus ; Respiratory Syncytial Virus, Human - immunology ; Respiratory Syncytial Virus, Human - pathogenicity ; Reverse Transcriptase Polymerase Chain Reaction ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Th1 Cells - immunology ; Th1 Cells - metabolism ; Th2 Cells - immunology ; Th2 Cells - metabolism ; Time Factors ; Tumor Necrosis Factor-alpha - metabolism ; Tumor Necrosis Factor-alpha - pharmacology ; Viral diseases ; Viral diseases of the respiratory system and ent viral diseases ; Virus Replication</subject><ispartof>International archives of allergy and immunology, 2011-01, Vol.154 (3), p.185-194</ispartof><rights>2010 S. Karger AG, Basel</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 S. Karger AG, Basel.</rights><rights>Copyright (c) 2011 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-a8de7ec56ffee97e4e46b1f4aab8d736ae486c485ee6bc76a1c7552f22fdd91a3</citedby><cites>FETCH-LOGICAL-c495t-a8de7ec56ffee97e4e46b1f4aab8d736ae486c485ee6bc76a1c7552f22fdd91a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23885460$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20861640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamada, Yumi</creatorcontrib><creatorcontrib>Matsumoto, Kenji</creatorcontrib><creatorcontrib>Hashimoto, Noriko</creatorcontrib><creatorcontrib>Saikusa, Miwako</creatorcontrib><creatorcontrib>Homma, Toshiki</creatorcontrib><creatorcontrib>Yoshihara, Shigemi</creatorcontrib><creatorcontrib>Saito, Hirohisa</creatorcontrib><title>Effect of Th1/Th2 Cytokine Pretreatment on RSV-Induced Gene Expression in Airway Epithelial Cells</title><title>International archives of allergy and immunology</title><addtitle>Int Arch Allergy Immunol</addtitle><description>Background: Respiratory syncytial virus (RSV) infection in infants with Th2 predisposition is thought to increase the risk of allergic sensitization, recurrent wheezing, and bronchial asthma during childhood. We attempted to clarify the molecular mechanisms by which Th1/Th2 predisposition in the host alters RSV infection and facilitates airway inflammation. Methods: A549 human airway epithelial cells were inoculated with live or UV-treated RSV after pretreatment with either a combination of tumor necrosis factor (TNF)-α and interferon-γ (Th1-primed) or a combination of TNF-α and interleukin-4 (Th2-primed) for 48 h. The gene and protein expression profiles of RSV-infected A549 cells were examined. Results: GeneChip analysis indicated that, at 96 h after inoculation with RSV, the expression of 62 genes was specifically enhanced (more than 2-fold by normalized data) in Th2-primed cells compared to that in unprimed or Th1-primed cells. An increase in mRNA and protein levels of monocyte chemoattractant protein (MCP)-1/CCL2 among those 62 genes was confirmed by real-time PCR and cytometric bead assay, respectively. RSV replication was markedly diminished in Th1-primed airway epithelial cells but not in Th2-primed cells, which was presumably caused at least in part by the early induction of antiviral genes. Conclusions: These results suggest that Th1/Th2 predisposition in the host prior to RSV infection critically regulates inflammatory reactions in the airways through alteration of gene expression, and that MCP-1/CCL2 plays an important role in the pathogenesis of severe RSV infection and the subsequent development of asthma in Th2-predisposed hosts.</description><subject>Asthma</subject><subject>Babies</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - virology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Immunopathology</subject><subject>Infectious diseases</subject><subject>Interferon-gamma - metabolism</subject><subject>Interferon-gamma - pharmacology</subject><subject>Lung - cytology</subject><subject>Lung - drug effects</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Lung - virology</subject><subject>Medical sciences</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Original Paper</subject><subject>Pathogenesis</subject><subject>Respiratory syncytial virus</subject><subject>Respiratory Syncytial Virus, Human - immunology</subject><subject>Respiratory Syncytial Virus, Human - pathogenicity</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Sarcoidosis. 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Psychology</topic><topic>Fundamental immunology</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Immunopathology</topic><topic>Infectious diseases</topic><topic>Interferon-gamma - metabolism</topic><topic>Interferon-gamma - pharmacology</topic><topic>Lung - cytology</topic><topic>Lung - drug effects</topic><topic>Lung - immunology</topic><topic>Lung - metabolism</topic><topic>Lung - virology</topic><topic>Medical sciences</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Original Paper</topic><topic>Pathogenesis</topic><topic>Respiratory syncytial virus</topic><topic>Respiratory Syncytial Virus, Human - immunology</topic><topic>Respiratory Syncytial Virus, Human - pathogenicity</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Th1 Cells - immunology</topic><topic>Th1 Cells - metabolism</topic><topic>Th2 Cells - immunology</topic><topic>Th2 Cells - metabolism</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Viral diseases</topic><topic>Viral diseases of the respiratory system and ent viral diseases</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamada, Yumi</creatorcontrib><creatorcontrib>Matsumoto, Kenji</creatorcontrib><creatorcontrib>Hashimoto, Noriko</creatorcontrib><creatorcontrib>Saikusa, Miwako</creatorcontrib><creatorcontrib>Homma, Toshiki</creatorcontrib><creatorcontrib>Yoshihara, Shigemi</creatorcontrib><creatorcontrib>Saito, Hirohisa</creatorcontrib><collection>Pascal-Francis</collection><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>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>International archives of allergy and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamada, Yumi</au><au>Matsumoto, Kenji</au><au>Hashimoto, Noriko</au><au>Saikusa, Miwako</au><au>Homma, Toshiki</au><au>Yoshihara, Shigemi</au><au>Saito, Hirohisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Th1/Th2 Cytokine Pretreatment on RSV-Induced Gene Expression in Airway Epithelial Cells</atitle><jtitle>International archives of allergy and immunology</jtitle><addtitle>Int Arch Allergy Immunol</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>154</volume><issue>3</issue><spage>185</spage><epage>194</epage><pages>185-194</pages><issn>1018-2438</issn><eissn>1423-0097</eissn><abstract>Background: Respiratory syncytial virus (RSV) infection in infants with Th2 predisposition is thought to increase the risk of allergic sensitization, recurrent wheezing, and bronchial asthma during childhood. We attempted to clarify the molecular mechanisms by which Th1/Th2 predisposition in the host alters RSV infection and facilitates airway inflammation. Methods: A549 human airway epithelial cells were inoculated with live or UV-treated RSV after pretreatment with either a combination of tumor necrosis factor (TNF)-α and interferon-γ (Th1-primed) or a combination of TNF-α and interleukin-4 (Th2-primed) for 48 h. The gene and protein expression profiles of RSV-infected A549 cells were examined. Results: GeneChip analysis indicated that, at 96 h after inoculation with RSV, the expression of 62 genes was specifically enhanced (more than 2-fold by normalized data) in Th2-primed cells compared to that in unprimed or Th1-primed cells. An increase in mRNA and protein levels of monocyte chemoattractant protein (MCP)-1/CCL2 among those 62 genes was confirmed by real-time PCR and cytometric bead assay, respectively. RSV replication was markedly diminished in Th1-primed airway epithelial cells but not in Th2-primed cells, which was presumably caused at least in part by the early induction of antiviral genes. Conclusions: These results suggest that Th1/Th2 predisposition in the host prior to RSV infection critically regulates inflammatory reactions in the airways through alteration of gene expression, and that MCP-1/CCL2 plays an important role in the pathogenesis of severe RSV infection and the subsequent development of asthma in Th2-predisposed hosts.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>20861640</pmid><doi>10.1159/000321105</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Karger Journals; MEDLINE; Alma/SFX Local Collection |
| subjects | Asthma Babies Biological and medical sciences Cell Line Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Cytokines - genetics Cytokines - metabolism Epithelial Cells - drug effects Epithelial Cells - immunology Epithelial Cells - metabolism Epithelial Cells - virology Fundamental and applied biological sciences. Psychology Fundamental immunology Gene Expression Profiling Gene Expression Regulation Human viral diseases Humans Immunopathology Infectious diseases Interferon-gamma - metabolism Interferon-gamma - pharmacology Lung - cytology Lung - drug effects Lung - immunology Lung - metabolism Lung - virology Medical sciences Oligonucleotide Array Sequence Analysis Original Paper Pathogenesis Respiratory syncytial virus Respiratory Syncytial Virus, Human - immunology Respiratory Syncytial Virus, Human - pathogenicity Reverse Transcriptase Polymerase Chain Reaction Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Th1 Cells - immunology Th1 Cells - metabolism Th2 Cells - immunology Th2 Cells - metabolism Time Factors Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factor-alpha - pharmacology Viral diseases Viral diseases of the respiratory system and ent viral diseases Virus Replication |
| title | Effect of Th1/Th2 Cytokine Pretreatment on RSV-Induced Gene Expression in Airway Epithelial Cells |
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