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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Veröffentlicht in:FEMS immunology and medical microbiology 2012-03, Vol.64 (2), p.273-279
Hauptverfasser: 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
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container_issue 2
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container_title FEMS immunology and medical microbiology
container_volume 64
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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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. 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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 &amp; 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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