The metalloporphyrin antioxidant, MnTE-2-PyP, inhibits Th2 cell immune responses in an asthma model
MnTE-2-PyP, a superoxide dismutase mimetic, inhibited OVA-induced airway inflammation in mice suggesting an effect on Th2 responsiveness. Thus, we hypothesized that MnTE-2-PyP may alter dendritic cell-Th2 interactions. Bone marrow derived dendritic cells (DC) and OVA(323-339)-specific Th2 cells were...
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description | MnTE-2-PyP, a superoxide dismutase mimetic, inhibited OVA-induced airway inflammation in mice suggesting an effect on Th2 responsiveness. Thus, we hypothesized that MnTE-2-PyP may alter dendritic cell-Th2 interactions. Bone marrow derived dendritic cells (DC) and OVA(323-339)-specific Th2 cells were cultured separately in the presence or absence of MnTE-2-PyP for 3 days prior to the co-culturing of the two cell types in the presence of an OVA(323-339) peptide and in some cases stimulated with CD3/CD28. MnTE-2-PyP-pretreated DC inhibited IL-4, IL-5 and IFNγ production and inhibited Th2 cell proliferation in the DC-Th2 co-culturing system in the presence of the OVA(323-339) peptide. Similar results were obtained using the CD3/CD28 cell-activation system; the addition of MnTE-2-PyP inhibited Th2 cell proliferation. MnTE-2-PyP suppressed CD25 expression on OVA-specific Th2 cells, which implied that MnTE-2-PyP can inhibit the activation of Th2 cells. MnTE-2-PyP also down-regulated co-stimulatory molecules: CD40, CD80 and CD86 on immature DC. Our studies suggest that the major mechanism by which MnTE-2-PyP inhibits airway inflammation is by acting on the DC and suppressing Th2 cell proliferation and activation. |
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Thus, we hypothesized that MnTE-2-PyP may alter dendritic cell-Th2 interactions. Bone marrow derived dendritic cells (DC) and OVA(323-339)-specific Th2 cells were cultured separately in the presence or absence of MnTE-2-PyP for 3 days prior to the co-culturing of the two cell types in the presence of an OVA(323-339) peptide and in some cases stimulated with CD3/CD28. MnTE-2-PyP-pretreated DC inhibited IL-4, IL-5 and IFNγ production and inhibited Th2 cell proliferation in the DC-Th2 co-culturing system in the presence of the OVA(323-339) peptide. Similar results were obtained using the CD3/CD28 cell-activation system; the addition of MnTE-2-PyP inhibited Th2 cell proliferation. MnTE-2-PyP suppressed CD25 expression on OVA-specific Th2 cells, which implied that MnTE-2-PyP can inhibit the activation of Th2 cells. MnTE-2-PyP also down-regulated co-stimulatory molecules: CD40, CD80 and CD86 on immature DC. Our studies suggest that the major mechanism by which MnTE-2-PyP inhibits airway inflammation is by acting on the DC and suppressing Th2 cell proliferation and activation.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms13089785</identifier><identifier>PMID: 22949830</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Airway management ; Allergens ; Allergies ; Animals ; Antigens ; Antioxidants ; Antioxidants - pharmacology ; Asthma ; Asthma - drug therapy ; Asthma - immunology ; Asthma - pathology ; Cell growth ; Cell Proliferation - drug effects ; Cells, Cultured ; Cytokines ; Dendritic cells ; Dendritic Cells - cytology ; Dendritic Cells - drug effects ; Dendritic Cells - immunology ; Disease Models, Animal ; Flow Cytometry ; Immune system ; Inflammation ; Lymphocytes ; Metalloporphyrins - pharmacology ; Mice ; Mice, Inbred BALB C ; Ovalbumin - pharmacology ; Pathogenesis ; Peptides ; Th2 Cells - drug effects ; Th2 Cells - immunology ; Th2 Cells - pathology</subject><ispartof>International journal of molecular sciences, 2012, Vol.13 (8), p.9785-9797</ispartof><rights>Copyright MDPI AG 2012</rights><rights>2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-54ca77b573e633c1b185695e07320543719d7f4a302f73a927cd247beb70521f3</citedby><cites>FETCH-LOGICAL-c412t-54ca77b573e633c1b185695e07320543719d7f4a302f73a927cd247beb70521f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431828/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431828/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22949830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jungsuwadee, Paiboon</creatorcontrib><creatorcontrib>Weaver, Michael R</creatorcontrib><creatorcontrib>Gally, Fabienne</creatorcontrib><creatorcontrib>Oberley-Deegan, Rebecca E</creatorcontrib><title>The metalloporphyrin antioxidant, MnTE-2-PyP, inhibits Th2 cell immune responses in an asthma model</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>MnTE-2-PyP, a superoxide dismutase mimetic, inhibited OVA-induced airway inflammation in mice suggesting an effect on Th2 responsiveness. Thus, we hypothesized that MnTE-2-PyP may alter dendritic cell-Th2 interactions. Bone marrow derived dendritic cells (DC) and OVA(323-339)-specific Th2 cells were cultured separately in the presence or absence of MnTE-2-PyP for 3 days prior to the co-culturing of the two cell types in the presence of an OVA(323-339) peptide and in some cases stimulated with CD3/CD28. MnTE-2-PyP-pretreated DC inhibited IL-4, IL-5 and IFNγ production and inhibited Th2 cell proliferation in the DC-Th2 co-culturing system in the presence of the OVA(323-339) peptide. Similar results were obtained using the CD3/CD28 cell-activation system; the addition of MnTE-2-PyP inhibited Th2 cell proliferation. MnTE-2-PyP suppressed CD25 expression on OVA-specific Th2 cells, which implied that MnTE-2-PyP can inhibit the activation of Th2 cells. MnTE-2-PyP also down-regulated co-stimulatory molecules: CD40, CD80 and CD86 on immature DC. Our studies suggest that the major mechanism by which MnTE-2-PyP inhibits airway inflammation is by acting on the DC and suppressing Th2 cell proliferation and activation.</description><subject>Airway management</subject><subject>Allergens</subject><subject>Allergies</subject><subject>Animals</subject><subject>Antigens</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Asthma</subject><subject>Asthma - drug therapy</subject><subject>Asthma - immunology</subject><subject>Asthma - pathology</subject><subject>Cell growth</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - cytology</subject><subject>Dendritic Cells - drug effects</subject><subject>Dendritic Cells - immunology</subject><subject>Disease Models, Animal</subject><subject>Flow Cytometry</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Lymphocytes</subject><subject>Metalloporphyrins - pharmacology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Ovalbumin - pharmacology</subject><subject>Pathogenesis</subject><subject>Peptides</subject><subject>Th2 Cells - drug effects</subject><subject>Th2 Cells - immunology</subject><subject>Th2 Cells - pathology</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpVkc1LxDAQxYMoft88S8DrVpOZZtNeBBG_QNHDeg5pm9osbVKTrrj_vdVdZT29gfnNmwePkBPOzhFzdmHnXeTIslxmYovs8xQgYWwqtzfmPXIQ45wxQBD5LtkDyNM8Q7ZPylljaGcG3ba-96FvlsE6qt1g_aetRp3QJze7SSB5Wb5MqHWNLewQ6awBWpq2pbbrFs7QYGLvXTSR_pxTHYem07TzlWmPyE6t22iO13pIXm9vZtf3yePz3cP11WNSphyGRKSllrIQEs0UseQFz8Q0F4ZJBCZSlDyvZJ1qZFBL1DnIsoJUFqaQTACv8ZBcrnz7RdGZqjRuCLpVfbCdDkvltVX_N8426s1_KEyRZ5CNBmdrg-DfFyYOau4XwY2ZFRcwZcAyFCM1WVFl8DEGU_994Ex9V6I2Kxnx081Uf_BvB_gFVcyHRA</recordid><startdate>2012</startdate><enddate>2012</enddate><creator>Jungsuwadee, Paiboon</creator><creator>Weaver, Michael R</creator><creator>Gally, Fabienne</creator><creator>Oberley-Deegan, Rebecca E</creator><general>MDPI AG</general><general>Molecular Diversity Preservation International (MDPI)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>2012</creationdate><title>The metalloporphyrin antioxidant, MnTE-2-PyP, inhibits Th2 cell immune responses in an asthma model</title><author>Jungsuwadee, Paiboon ; Weaver, Michael R ; Gally, Fabienne ; Oberley-Deegan, Rebecca E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-54ca77b573e633c1b185695e07320543719d7f4a302f73a927cd247beb70521f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Airway management</topic><topic>Allergens</topic><topic>Allergies</topic><topic>Animals</topic><topic>Antigens</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Asthma</topic><topic>Asthma - drug therapy</topic><topic>Asthma - immunology</topic><topic>Asthma - pathology</topic><topic>Cell growth</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - cytology</topic><topic>Dendritic Cells - drug effects</topic><topic>Dendritic Cells - immunology</topic><topic>Disease Models, Animal</topic><topic>Flow Cytometry</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Lymphocytes</topic><topic>Metalloporphyrins - pharmacology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Ovalbumin - pharmacology</topic><topic>Pathogenesis</topic><topic>Peptides</topic><topic>Th2 Cells - drug effects</topic><topic>Th2 Cells - immunology</topic><topic>Th2 Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jungsuwadee, Paiboon</creatorcontrib><creatorcontrib>Weaver, Michael R</creatorcontrib><creatorcontrib>Gally, Fabienne</creatorcontrib><creatorcontrib>Oberley-Deegan, Rebecca E</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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 China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jungsuwadee, Paiboon</au><au>Weaver, Michael R</au><au>Gally, Fabienne</au><au>Oberley-Deegan, Rebecca E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The metalloporphyrin antioxidant, MnTE-2-PyP, inhibits Th2 cell immune responses in an asthma model</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2012</date><risdate>2012</risdate><volume>13</volume><issue>8</issue><spage>9785</spage><epage>9797</epage><pages>9785-9797</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>MnTE-2-PyP, a superoxide dismutase mimetic, inhibited OVA-induced airway inflammation in mice suggesting an effect on Th2 responsiveness. Thus, we hypothesized that MnTE-2-PyP may alter dendritic cell-Th2 interactions. Bone marrow derived dendritic cells (DC) and OVA(323-339)-specific Th2 cells were cultured separately in the presence or absence of MnTE-2-PyP for 3 days prior to the co-culturing of the two cell types in the presence of an OVA(323-339) peptide and in some cases stimulated with CD3/CD28. MnTE-2-PyP-pretreated DC inhibited IL-4, IL-5 and IFNγ production and inhibited Th2 cell proliferation in the DC-Th2 co-culturing system in the presence of the OVA(323-339) peptide. Similar results were obtained using the CD3/CD28 cell-activation system; the addition of MnTE-2-PyP inhibited Th2 cell proliferation. MnTE-2-PyP suppressed CD25 expression on OVA-specific Th2 cells, which implied that MnTE-2-PyP can inhibit the activation of Th2 cells. MnTE-2-PyP also down-regulated co-stimulatory molecules: CD40, CD80 and CD86 on immature DC. Our studies suggest that the major mechanism by which MnTE-2-PyP inhibits airway inflammation is by acting on the DC and suppressing Th2 cell proliferation and activation.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>22949830</pmid><doi>10.3390/ijms13089785</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Airway management Allergens Allergies Animals Antigens Antioxidants Antioxidants - pharmacology Asthma Asthma - drug therapy Asthma - immunology Asthma - pathology Cell growth Cell Proliferation - drug effects Cells, Cultured Cytokines Dendritic cells Dendritic Cells - cytology Dendritic Cells - drug effects Dendritic Cells - immunology Disease Models, Animal Flow Cytometry Immune system Inflammation Lymphocytes Metalloporphyrins - pharmacology Mice Mice, Inbred BALB C Ovalbumin - pharmacology Pathogenesis Peptides Th2 Cells - drug effects Th2 Cells - immunology Th2 Cells - pathology |
title | The metalloporphyrin antioxidant, MnTE-2-PyP, inhibits Th2 cell immune responses in an asthma model |
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