Hydrogen Peroxide Reverses IL-5 Afforded Eosinophil Survival and Promotes Constitutive Human Eosinophil Apoptosis
Background: Eosinophils play a central role in the induction and perpetuation of allergic inflammatory responses. The present study was performed to investigate the effects of reactive oxygen intermediates on constitutive apoptosis as well as on interleukin (IL)-5 afforded human eosinophil survival....
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| Veröffentlicht in: | International archives of allergy and immunology 2002-01, Vol.127 (1), p.73-78 |
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| container_title | International archives of allergy and immunology |
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| creator | Kankaanranta, Hannu Giembycz, Mark A. Barnes, Peter J. Haddad, El-Bdaoui Saarelainen, Seppo Zhang, Xianzhi Moilanen, Eeva Lindsay, Mark A. |
| description | Background: Eosinophils play a central role in the induction and perpetuation of allergic inflammatory responses. The present study was performed to investigate the effects of reactive oxygen intermediates on constitutive apoptosis as well as on interleukin (IL)-5 afforded human eosinophil survival. Methods: Peripheral blood eosinophils were isolated by CD16-negative selection to >99% purity and were cultured for 48 h. The number of apoptotic eosinophils in the culture was assessed by flow cytometric analysis of relative DNA content in propidium-iodide-stained cells, annexin-V binding or by morphological analysis. Apoptosis was confirmed by the appearance of a typical ladder pattern in the DNA fragmentation assay by agarose gel electrophoresis. Results: Exogenous H 2 O 2 reversed IL-5-afforded eosinophil survival by inducing apoptosis. Constitutive eosinophil apoptosis was inhibited by a reduction of intracellular levels of H 2 O 2 by catalase. Exogenous H 2 O 2 increased the rate of constitutive apoptosis. Conclusions: Our results suggest that H 2 O 2 may play a role in the downregulation of eosinophilic inflammation by inducing eosinophil apoptosis. |
| doi_str_mv | 10.1159/000048171 |
| format | Article |
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The present study was performed to investigate the effects of reactive oxygen intermediates on constitutive apoptosis as well as on interleukin (IL)-5 afforded human eosinophil survival. Methods: Peripheral blood eosinophils were isolated by CD16-negative selection to >99% purity and were cultured for 48 h. The number of apoptotic eosinophils in the culture was assessed by flow cytometric analysis of relative DNA content in propidium-iodide-stained cells, annexin-V binding or by morphological analysis. Apoptosis was confirmed by the appearance of a typical ladder pattern in the DNA fragmentation assay by agarose gel electrophoresis. Results: Exogenous H 2 O 2 reversed IL-5-afforded eosinophil survival by inducing apoptosis. Constitutive eosinophil apoptosis was inhibited by a reduction of intracellular levels of H 2 O 2 by catalase. Exogenous H 2 O 2 increased the rate of constitutive apoptosis. Conclusions: Our results suggest that H 2 O 2 may play a role in the downregulation of eosinophilic inflammation by inducing eosinophil apoptosis.</description><identifier>ISSN: 1018-2438</identifier><identifier>EISSN: 1423-0097</identifier><identifier>DOI: 10.1159/000048171</identifier><identifier>PMID: 11893856</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Allergic diseases ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Catalase - metabolism ; Cells, Cultured ; Eosinophils - drug effects ; Eosinophils - physiology ; fas Receptor - metabolism ; General aspects ; Humans ; Hydrogen Peroxide - pharmacology ; Immunopathology ; Interleukin-5 - physiology ; Medical sciences ; Original Paper</subject><ispartof>International archives of allergy and immunology, 2002-01, Vol.127 (1), p.73-78</ispartof><rights>2002 S. Karger AG, Basel</rights><rights>2002 INIST-CNRS</rights><rights>Copyright (c) 2002 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-a164eabeb7286d77cc1062f460540059f52574e04c7335e26a020c172fcfb7183</citedby><cites>FETCH-LOGICAL-c385t-a164eabeb7286d77cc1062f460540059f52574e04c7335e26a020c172fcfb7183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,2425,4012,27910,27911,27912</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13551155$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11893856$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kankaanranta, Hannu</creatorcontrib><creatorcontrib>Giembycz, Mark A.</creatorcontrib><creatorcontrib>Barnes, Peter J.</creatorcontrib><creatorcontrib>Haddad, El-Bdaoui</creatorcontrib><creatorcontrib>Saarelainen, Seppo</creatorcontrib><creatorcontrib>Zhang, Xianzhi</creatorcontrib><creatorcontrib>Moilanen, Eeva</creatorcontrib><creatorcontrib>Lindsay, Mark A.</creatorcontrib><title>Hydrogen Peroxide Reverses IL-5 Afforded Eosinophil Survival and Promotes Constitutive Human Eosinophil Apoptosis</title><title>International archives of allergy and immunology</title><addtitle>Int Arch Allergy Immunol</addtitle><description>Background: Eosinophils play a central role in the induction and perpetuation of allergic inflammatory responses. The present study was performed to investigate the effects of reactive oxygen intermediates on constitutive apoptosis as well as on interleukin (IL)-5 afforded human eosinophil survival. Methods: Peripheral blood eosinophils were isolated by CD16-negative selection to >99% purity and were cultured for 48 h. The number of apoptotic eosinophils in the culture was assessed by flow cytometric analysis of relative DNA content in propidium-iodide-stained cells, annexin-V binding or by morphological analysis. Apoptosis was confirmed by the appearance of a typical ladder pattern in the DNA fragmentation assay by agarose gel electrophoresis. Results: Exogenous H 2 O 2 reversed IL-5-afforded eosinophil survival by inducing apoptosis. Constitutive eosinophil apoptosis was inhibited by a reduction of intracellular levels of H 2 O 2 by catalase. Exogenous H 2 O 2 increased the rate of constitutive apoptosis. Conclusions: Our results suggest that H 2 O 2 may play a role in the downregulation of eosinophilic inflammation by inducing eosinophil apoptosis.</description><subject>Allergic diseases</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Catalase - metabolism</subject><subject>Cells, Cultured</subject><subject>Eosinophils - drug effects</subject><subject>Eosinophils - physiology</subject><subject>fas Receptor - metabolism</subject><subject>General aspects</subject><subject>Humans</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Immunopathology</subject><subject>Interleukin-5 - physiology</subject><subject>Medical sciences</subject><subject>Original Paper</subject><issn>1018-2438</issn><issn>1423-0097</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpt0dtLHDEUB-BQKvXWhz4XShAq-DCay2SSfRwWdRcWFC_PQzZzYmNnJmMys9T_3ugubhHzkgS-nPMjB6EflJxSKiZnJK1cUUm_oD2aM54RMpFf05lQlbGcq120H-MjIQmr4hvapVRNuBLFHnqaPdfBP0CHryH4f64GfAMrCBEini8ygUtrfaihxuc-us73f1yDb8ewcivdYN3V-Dr41g-JT30XBzeMg1sBno2t7v5_U_a-H9I1HqIdq5sI3zf7Abq_OL-bzrLF1eV8Wi4yk5INmaZFDnoJS8lUUUtpDCUFs3lBRE6ImFjBhMyB5EZyLoAVmjBiqGTW2KWkih-g43XdPvinEeJQtS4aaBrdgR9jlYgquKIJHn2Aj34MXcpWMUYVE4q_opM1MsHHGMBWfXCtDs8VJdXrEKr3IST7a1NwXLZQb-Xm1xP4vQE6Gt3YoDvj4tZxIVJJsU32V4cHCO9gXpZvnaq-tgn9_BSts7wAojSiOw</recordid><startdate>200201</startdate><enddate>200201</enddate><creator>Kankaanranta, Hannu</creator><creator>Giembycz, Mark A.</creator><creator>Barnes, Peter J.</creator><creator>Haddad, El-Bdaoui</creator><creator>Saarelainen, Seppo</creator><creator>Zhang, Xianzhi</creator><creator>Moilanen, Eeva</creator><creator>Lindsay, Mark A.</creator><general>Karger</general><general>S. 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Giembycz, Mark A. ; Barnes, Peter J. ; Haddad, El-Bdaoui ; Saarelainen, Seppo ; Zhang, Xianzhi ; Moilanen, Eeva ; Lindsay, Mark A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-a164eabeb7286d77cc1062f460540059f52574e04c7335e26a020c172fcfb7183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Allergic diseases</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Catalase - metabolism</topic><topic>Cells, Cultured</topic><topic>Eosinophils - drug effects</topic><topic>Eosinophils - physiology</topic><topic>fas Receptor - metabolism</topic><topic>General aspects</topic><topic>Humans</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Immunopathology</topic><topic>Interleukin-5 - physiology</topic><topic>Medical sciences</topic><topic>Original Paper</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kankaanranta, Hannu</creatorcontrib><creatorcontrib>Giembycz, Mark A.</creatorcontrib><creatorcontrib>Barnes, Peter J.</creatorcontrib><creatorcontrib>Haddad, El-Bdaoui</creatorcontrib><creatorcontrib>Saarelainen, Seppo</creatorcontrib><creatorcontrib>Zhang, Xianzhi</creatorcontrib><creatorcontrib>Moilanen, Eeva</creatorcontrib><creatorcontrib>Lindsay, Mark A.</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 One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><jtitle>International archives of allergy and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kankaanranta, Hannu</au><au>Giembycz, Mark A.</au><au>Barnes, Peter J.</au><au>Haddad, El-Bdaoui</au><au>Saarelainen, Seppo</au><au>Zhang, Xianzhi</au><au>Moilanen, Eeva</au><au>Lindsay, Mark A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydrogen Peroxide Reverses IL-5 Afforded Eosinophil Survival and Promotes Constitutive Human Eosinophil Apoptosis</atitle><jtitle>International archives of allergy and immunology</jtitle><addtitle>Int Arch Allergy Immunol</addtitle><date>2002-01</date><risdate>2002</risdate><volume>127</volume><issue>1</issue><spage>73</spage><epage>78</epage><pages>73-78</pages><issn>1018-2438</issn><eissn>1423-0097</eissn><abstract>Background: Eosinophils play a central role in the induction and perpetuation of allergic inflammatory responses. The present study was performed to investigate the effects of reactive oxygen intermediates on constitutive apoptosis as well as on interleukin (IL)-5 afforded human eosinophil survival. Methods: Peripheral blood eosinophils were isolated by CD16-negative selection to >99% purity and were cultured for 48 h. The number of apoptotic eosinophils in the culture was assessed by flow cytometric analysis of relative DNA content in propidium-iodide-stained cells, annexin-V binding or by morphological analysis. Apoptosis was confirmed by the appearance of a typical ladder pattern in the DNA fragmentation assay by agarose gel electrophoresis. Results: Exogenous H 2 O 2 reversed IL-5-afforded eosinophil survival by inducing apoptosis. Constitutive eosinophil apoptosis was inhibited by a reduction of intracellular levels of H 2 O 2 by catalase. Exogenous H 2 O 2 increased the rate of constitutive apoptosis. Conclusions: Our results suggest that H 2 O 2 may play a role in the downregulation of eosinophilic inflammation by inducing eosinophil apoptosis.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>11893856</pmid><doi>10.1159/000048171</doi><tpages>6</tpages></addata></record> |
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| subjects | Allergic diseases Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Catalase - metabolism Cells, Cultured Eosinophils - drug effects Eosinophils - physiology fas Receptor - metabolism General aspects Humans Hydrogen Peroxide - pharmacology Immunopathology Interleukin-5 - physiology Medical sciences Original Paper |
| title | Hydrogen Peroxide Reverses IL-5 Afforded Eosinophil Survival and Promotes Constitutive Human Eosinophil Apoptosis |
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