Concanavalin-A induces IL-17 production during the course of Candida albicans infection
Abstract In a previous study, our group verified that 100% of mice survived to a lethal dose of Candida albicans following pretreatment with concanavalin-A (Con-A) for 3 days. This work proposed to investigate whether treatment could mediate an adaptative immune response involving TH17 cells. A sign...
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creator | de Carvalho, Paula Galdino Cardin Custódio, Luiz Antonio Conchon-Costa, Ivete de Jesus Andrade, Célia Guadalupe Tardeli Quirino, Gustavo Fernando da Silva de Almeida, Ricardo Sergio Couto Felipe, Ionice |
description | Abstract
In a previous study, our group verified that 100% of mice survived to a lethal dose of Candida albicans following pretreatment with concanavalin-A (Con-A) for 3 days. This work proposed to investigate whether treatment could mediate an adaptative immune response involving TH17 cells. A significant increase in IL-17 levels at 6 h postinfection was observed and was maintained up to 18 h in the Con-A group, whereas in control mice, a reduction in this cytokine was verified. In addition, TH17 cells develop in the presence of TGF-β, IL-1 β, and IL-6 that were increased significantly 2 h postinfection in Con-A-treated mice. Macrophages were involved in the process, engulfing greater numbers of yeast cells, and were activated through TNF-α and interferon-γ produced at significant levels at 2 h postinfection. A significant increase in IL-12 levels was also observed at 2 h postinfection. Thus, activated macrophages were probably more capable of killing and processing Candida antigens, signalizing an adaptative immune response. Macrophages from controls did not prevent yeast-to-hyphae transition and were partially destroyed, as shown in scanning microscopy. These results suggest that treatment with Con-A facilitated the triggering of TH17 and TH1 responses via IL-17 and IFN-γ production, leading to the resolution of C. albicans infection. |
doi_str_mv | 10.1111/j.1574-695X.2011.00904.x |
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In a previous study, our group verified that 100% of mice survived to a lethal dose of Candida albicans following pretreatment with concanavalin-A (Con-A) for 3 days. This work proposed to investigate whether treatment could mediate an adaptative immune response involving TH17 cells. A significant increase in IL-17 levels at 6 h postinfection was observed and was maintained up to 18 h in the Con-A group, whereas in control mice, a reduction in this cytokine was verified. In addition, TH17 cells develop in the presence of TGF-β, IL-1 β, and IL-6 that were increased significantly 2 h postinfection in Con-A-treated mice. Macrophages were involved in the process, engulfing greater numbers of yeast cells, and were activated through TNF-α and interferon-γ produced at significant levels at 2 h postinfection. A significant increase in IL-12 levels was also observed at 2 h postinfection. Thus, activated macrophages were probably more capable of killing and processing Candida antigens, signalizing an adaptative immune response. Macrophages from controls did not prevent yeast-to-hyphae transition and were partially destroyed, as shown in scanning microscopy. These results suggest that treatment with Con-A facilitated the triggering of TH17 and TH1 responses via IL-17 and IFN-γ production, leading to the resolution of C. albicans infection.</description><identifier>ISSN: 0928-8244</identifier><identifier>EISSN: 1574-695X</identifier><identifier>EISSN: 2049-632X</identifier><identifier>DOI: 10.1111/j.1574-695X.2011.00904.x</identifier><identifier>PMID: 22098271</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Antigen processing ; Antigens ; Ascitic Fluid - cytology ; Biological and medical sciences ; Candida albicans ; Candida albicans - immunology ; Candida albicans infection ; Candidiasis - drug therapy ; Candidiasis - immunology ; Candidiasis - metabolism ; Concanavalin A - pharmacology ; concanavalin‐A ; Cytokines - biosynthesis ; Cytokines - immunology ; Fundamental and applied biological sciences. Psychology ; gamma -Interferon ; Helper cells ; Hyphae ; Immune response ; Immune system ; Infection ; Information processing ; Interferon ; Interleukin 1 ; Interleukin 12 ; Interleukin 17 ; Interleukin 6 ; Interleukin-17 - biosynthesis ; Interleukin-17 - immunology ; Lethal dose ; Lymphocytes T ; Macrophages ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - microbiology ; Male ; Mice ; Microbiology ; Miscellaneous ; Mycology ; Phagocytosis - drug effects ; Phagocytosis - immunology ; Pretreatment ; Scanning ; Scanning microscopy ; TH1 and TH17 immune response ; Th1 Cells - immunology ; Th1 Cells - metabolism ; Th17 Cells - immunology ; Th17 Cells - metabolism ; Transforming growth factor- beta ; Tumor necrosis factor- alpha ; Tumor necrosis factor-α ; Yeast ; Yeasts ; γ-Interferon</subject><ispartof>FEMS immunology and medical microbiology, 2012-03, Vol.64 (2), p.273-279</ispartof><rights>2011 Federation of European Microbiological Societies. 2011</rights><rights>2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved</rights><rights>2015 INIST-CNRS</rights><rights>2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.</rights><rights>2011 Federation of European Microbiological Societies.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5014-fd29b692f52b8994258ab1bd44791df7850d284f503a0e0c7d097d511fa8b84b3</citedby><cites>FETCH-LOGICAL-c5014-fd29b692f52b8994258ab1bd44791df7850d284f503a0e0c7d097d511fa8b84b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1574-695X.2011.00904.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1574-695X.2011.00904.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27931,27932,45581,45582</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25502531$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22098271$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Carvalho, Paula Galdino Cardin</creatorcontrib><creatorcontrib>Custódio, Luiz Antonio</creatorcontrib><creatorcontrib>Conchon-Costa, Ivete</creatorcontrib><creatorcontrib>de Jesus Andrade, Célia Guadalupe Tardeli</creatorcontrib><creatorcontrib>Quirino, Gustavo Fernando da Silva</creatorcontrib><creatorcontrib>de Almeida, Ricardo Sergio Couto</creatorcontrib><creatorcontrib>Felipe, Ionice</creatorcontrib><title>Concanavalin-A induces IL-17 production during the course of Candida albicans infection</title><title>FEMS immunology and medical microbiology</title><addtitle>FEMS Immunol Med Microbiol</addtitle><description>Abstract
In a previous study, our group verified that 100% of mice survived to a lethal dose of Candida albicans following pretreatment with concanavalin-A (Con-A) for 3 days. This work proposed to investigate whether treatment could mediate an adaptative immune response involving TH17 cells. A significant increase in IL-17 levels at 6 h postinfection was observed and was maintained up to 18 h in the Con-A group, whereas in control mice, a reduction in this cytokine was verified. In addition, TH17 cells develop in the presence of TGF-β, IL-1 β, and IL-6 that were increased significantly 2 h postinfection in Con-A-treated mice. Macrophages were involved in the process, engulfing greater numbers of yeast cells, and were activated through TNF-α and interferon-γ produced at significant levels at 2 h postinfection. A significant increase in IL-12 levels was also observed at 2 h postinfection. Thus, activated macrophages were probably more capable of killing and processing Candida antigens, signalizing an adaptative immune response. Macrophages from controls did not prevent yeast-to-hyphae transition and were partially destroyed, as shown in scanning microscopy. These results suggest that treatment with Con-A facilitated the triggering of TH17 and TH1 responses via IL-17 and IFN-γ production, leading to the resolution of C. albicans infection.</description><subject>Animals</subject><subject>Antigen processing</subject><subject>Antigens</subject><subject>Ascitic Fluid - cytology</subject><subject>Biological and medical sciences</subject><subject>Candida albicans</subject><subject>Candida albicans - immunology</subject><subject>Candida albicans infection</subject><subject>Candidiasis - drug therapy</subject><subject>Candidiasis - immunology</subject><subject>Candidiasis - metabolism</subject><subject>Concanavalin A - pharmacology</subject><subject>concanavalin‐A</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - immunology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>gamma -Interferon</subject><subject>Helper cells</subject><subject>Hyphae</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Infection</subject><subject>Information processing</subject><subject>Interferon</subject><subject>Interleukin 1</subject><subject>Interleukin 12</subject><subject>Interleukin 17</subject><subject>Interleukin 6</subject><subject>Interleukin-17 - biosynthesis</subject><subject>Interleukin-17 - immunology</subject><subject>Lethal dose</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - microbiology</subject><subject>Male</subject><subject>Mice</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>Mycology</subject><subject>Phagocytosis - drug effects</subject><subject>Phagocytosis - immunology</subject><subject>Pretreatment</subject><subject>Scanning</subject><subject>Scanning microscopy</subject><subject>TH1 and TH17 immune response</subject><subject>Th1 Cells - immunology</subject><subject>Th1 Cells - metabolism</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - metabolism</subject><subject>Transforming growth factor- beta</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumor necrosis factor-α</subject><subject>Yeast</subject><subject>Yeasts</subject><subject>γ-Interferon</subject><issn>0928-8244</issn><issn>1574-695X</issn><issn>2049-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkdFqFDEUhoModq2-ggREvJrxnEwyk4A3ZbF2YaU3Fb0LmUmiWWYz62Sntm9vprutoAjNTRLy_Sfn8BFCEUrM6_2mRNHwolbiW8kAsQRQwMubJ2Tx8PCULEAxWUjG-Ql5kdIGALgCeE5OGAMlWYML8nU5xM5Ec236EIszGqKdOpfoal1gQ3fjkK_7MERqpzHE73T_w9FumMbk6ODp0kQbrKGmb0OuknLcuzv-JXnmTZ_cq-N-Sr6cf7xaXhTry0-r5dm66AQgL7xlqq0V84K1UinOhDQttpbzRqH1jRRgmeReQGXAQddYUI0ViN7IVvK2OiXvDnVzqz8nl_Z6G1Ln-t5EN0xJK1ZLKWqsHkEiclmzOpNv_iI3eeKYx9CsgppVrEbMlDxQ3TikNDqvd2PYmvFWI-jZkt7oWYaeZejZkr6zpG9y9PXxg6ndOvsQvNeSgbdHwKTO9H40sQvpDycEMFHN3IcD9yv07vbRDejz1ed8yPHqEB-m3X_Cxb_d_wZR9Loh</recordid><startdate>201203</startdate><enddate>201203</enddate><creator>de Carvalho, Paula Galdino Cardin</creator><creator>Custódio, Luiz Antonio</creator><creator>Conchon-Costa, Ivete</creator><creator>de Jesus Andrade, Célia Guadalupe Tardeli</creator><creator>Quirino, Gustavo Fernando da Silva</creator><creator>de Almeida, Ricardo Sergio Couto</creator><creator>Felipe, Ionice</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Oxford University Press</general><scope>IQODW</scope><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>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope><scope>M7N</scope></search><sort><creationdate>201203</creationdate><title>Concanavalin-A induces IL-17 production during the course of Candida albicans infection</title><author>de Carvalho, Paula Galdino Cardin ; Custódio, Luiz Antonio ; Conchon-Costa, Ivete ; de Jesus Andrade, Célia Guadalupe Tardeli ; Quirino, Gustavo Fernando da Silva ; de Almeida, Ricardo Sergio Couto ; Felipe, Ionice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5014-fd29b692f52b8994258ab1bd44791df7850d284f503a0e0c7d097d511fa8b84b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Antigen processing</topic><topic>Antigens</topic><topic>Ascitic Fluid - cytology</topic><topic>Biological and medical sciences</topic><topic>Candida albicans</topic><topic>Candida albicans - immunology</topic><topic>Candida albicans infection</topic><topic>Candidiasis - drug therapy</topic><topic>Candidiasis - immunology</topic><topic>Candidiasis - metabolism</topic><topic>Concanavalin A - pharmacology</topic><topic>concanavalin‐A</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - immunology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>gamma -Interferon</topic><topic>Helper cells</topic><topic>Hyphae</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Infection</topic><topic>Information processing</topic><topic>Interferon</topic><topic>Interleukin 1</topic><topic>Interleukin 12</topic><topic>Interleukin 17</topic><topic>Interleukin 6</topic><topic>Interleukin-17 - biosynthesis</topic><topic>Interleukin-17 - immunology</topic><topic>Lethal dose</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - microbiology</topic><topic>Male</topic><topic>Mice</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>Mycology</topic><topic>Phagocytosis - drug effects</topic><topic>Phagocytosis - immunology</topic><topic>Pretreatment</topic><topic>Scanning</topic><topic>Scanning microscopy</topic><topic>TH1 and TH17 immune response</topic><topic>Th1 Cells - immunology</topic><topic>Th1 Cells - metabolism</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - metabolism</topic><topic>Transforming growth factor- beta</topic><topic>Tumor necrosis factor- alpha</topic><topic>Tumor necrosis factor-α</topic><topic>Yeast</topic><topic>Yeasts</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Carvalho, Paula Galdino Cardin</creatorcontrib><creatorcontrib>Custódio, Luiz Antonio</creatorcontrib><creatorcontrib>Conchon-Costa, Ivete</creatorcontrib><creatorcontrib>de Jesus Andrade, Célia Guadalupe Tardeli</creatorcontrib><creatorcontrib>Quirino, Gustavo Fernando da Silva</creatorcontrib><creatorcontrib>de Almeida, Ricardo Sergio Couto</creatorcontrib><creatorcontrib>Felipe, Ionice</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>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>FEMS immunology and medical microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Carvalho, Paula Galdino Cardin</au><au>Custódio, Luiz Antonio</au><au>Conchon-Costa, Ivete</au><au>de Jesus Andrade, Célia Guadalupe Tardeli</au><au>Quirino, Gustavo Fernando da Silva</au><au>de Almeida, Ricardo Sergio Couto</au><au>Felipe, Ionice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Concanavalin-A induces IL-17 production during the course of Candida albicans infection</atitle><jtitle>FEMS immunology and medical microbiology</jtitle><addtitle>FEMS Immunol Med Microbiol</addtitle><date>2012-03</date><risdate>2012</risdate><volume>64</volume><issue>2</issue><spage>273</spage><epage>279</epage><pages>273-279</pages><issn>0928-8244</issn><eissn>1574-695X</eissn><eissn>2049-632X</eissn><abstract>Abstract
In a previous study, our group verified that 100% of mice survived to a lethal dose of Candida albicans following pretreatment with concanavalin-A (Con-A) for 3 days. This work proposed to investigate whether treatment could mediate an adaptative immune response involving TH17 cells. A significant increase in IL-17 levels at 6 h postinfection was observed and was maintained up to 18 h in the Con-A group, whereas in control mice, a reduction in this cytokine was verified. In addition, TH17 cells develop in the presence of TGF-β, IL-1 β, and IL-6 that were increased significantly 2 h postinfection in Con-A-treated mice. Macrophages were involved in the process, engulfing greater numbers of yeast cells, and were activated through TNF-α and interferon-γ produced at significant levels at 2 h postinfection. A significant increase in IL-12 levels was also observed at 2 h postinfection. Thus, activated macrophages were probably more capable of killing and processing Candida antigens, signalizing an adaptative immune response. Macrophages from controls did not prevent yeast-to-hyphae transition and were partially destroyed, as shown in scanning microscopy. These results suggest that treatment with Con-A facilitated the triggering of TH17 and TH1 responses via IL-17 and IFN-γ production, leading to the resolution of C. albicans infection.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22098271</pmid><doi>10.1111/j.1574-695X.2011.00904.x</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Antigen processing Antigens Ascitic Fluid - cytology Biological and medical sciences Candida albicans Candida albicans - immunology Candida albicans infection Candidiasis - drug therapy Candidiasis - immunology Candidiasis - metabolism Concanavalin A - pharmacology concanavalin‐A Cytokines - biosynthesis Cytokines - immunology Fundamental and applied biological sciences. Psychology gamma -Interferon Helper cells Hyphae Immune response Immune system Infection Information processing Interferon Interleukin 1 Interleukin 12 Interleukin 17 Interleukin 6 Interleukin-17 - biosynthesis Interleukin-17 - immunology Lethal dose Lymphocytes T Macrophages Macrophages - cytology Macrophages - drug effects Macrophages - microbiology Male Mice Microbiology Miscellaneous Mycology Phagocytosis - drug effects Phagocytosis - immunology Pretreatment Scanning Scanning microscopy TH1 and TH17 immune response Th1 Cells - immunology Th1 Cells - metabolism Th17 Cells - immunology Th17 Cells - metabolism Transforming growth factor- beta Tumor necrosis factor- alpha Tumor necrosis factor-α Yeast Yeasts γ-Interferon |
title | Concanavalin-A induces IL-17 production during the course of Candida albicans infection |
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