TLR-Dependent Induction of IFN-beta Mediates Host Defense against Trypanosoma cruzi
Host resistance to the intracellular protozoan parasite Trypanosoma cruzi depends on IFN-gamma production by T cells and NK cells. However, the involvement of innate immunity in host resistance to T. cruzi remains unclear. In the present study, we investigated host defense against T. cruzi by focusi...
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| Veröffentlicht in: | Journal of Immunology 2006-11, Vol.177 (10), p.7059-7066 |
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| creator | Koga, Ritsuko Hamano, Shinjiro Kuwata, Hirotaka Atarashi, Koji Ogawa, Masahiro Hisaeda, Hajime Yamamoto, Masahiro Akira, Shizuo Himeno, Kunisuke Matsumoto, Makoto Takeda, Kiyoshi |
| description | Host resistance to the intracellular protozoan parasite Trypanosoma cruzi depends on IFN-gamma production by T cells and NK cells. However, the involvement of innate immunity in host resistance to T. cruzi remains unclear. In the present study, we investigated host defense against T. cruzi by focusing on innate immunity. Macrophages and dendritic cells (DCs) from MyD88(-/-)TRIF(-/-) mice, in which TLR-dependent activation of innate immunity was abolished, were defective in the clearance of T. cruzi and showed impaired induction of IFN-beta during T. cruzi infection. Neutralization of IFN-beta in MyD88(-/-) macrophages led to enhanced T. cruzi growth. Cells from MyD88(-/-)IFNAR1(-/-) mice also showed impaired T. cruzi clearance. Furthermore, both MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) mice were highly susceptible to in vivo T. cruzi infection, highlighting the involvement of innate immune responses in T. cruzi infection. We further analyzed the molecular mechanisms for the IFN-beta-mediated antitrypanosomal innate immune responses. MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) macrophages and DCs exhibited defective induction of the GTPase IFN-inducible p47 (IRG47) after T. cruzi infection. RNA interference-mediated reduction of IRG47 expression in MyD88(-/-) macrophages resulted in increased intracellular growth of T. cruzi. These findings suggest that TLR-dependent expression of IFN-beta is involved in resistance to T. cruzi infection through the induction of IRG47. |
| doi_str_mv | 10.4049/jimmunol.177.10.7059 |
| format | Article |
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However, the involvement of innate immunity in host resistance to T. cruzi remains unclear. In the present study, we investigated host defense against T. cruzi by focusing on innate immunity. Macrophages and dendritic cells (DCs) from MyD88(-/-)TRIF(-/-) mice, in which TLR-dependent activation of innate immunity was abolished, were defective in the clearance of T. cruzi and showed impaired induction of IFN-beta during T. cruzi infection. Neutralization of IFN-beta in MyD88(-/-) macrophages led to enhanced T. cruzi growth. Cells from MyD88(-/-)IFNAR1(-/-) mice also showed impaired T. cruzi clearance. Furthermore, both MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) mice were highly susceptible to in vivo T. cruzi infection, highlighting the involvement of innate immune responses in T. cruzi infection. We further analyzed the molecular mechanisms for the IFN-beta-mediated antitrypanosomal innate immune responses. MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) macrophages and DCs exhibited defective induction of the GTPase IFN-inducible p47 (IRG47) after T. cruzi infection. RNA interference-mediated reduction of IRG47 expression in MyD88(-/-) macrophages resulted in increased intracellular growth of T. cruzi. These findings suggest that TLR-dependent expression of IFN-beta is involved in resistance to T. cruzi infection through the induction of IRG47.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.4049/jimmunol.177.10.7059</identifier><identifier>PMID: 17082622</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Adaptor Proteins, Vesicular Transport - deficiency ; Adaptor Proteins, Vesicular Transport - genetics ; Animals ; Cells, Cultured ; Chagas Disease - genetics ; Chagas Disease - immunology ; Chagas Disease - parasitology ; Dendritic Cells - immunology ; Dendritic Cells - metabolism ; Dendritic Cells - parasitology ; Gene Expression Regulation - immunology ; Growth Inhibitors - biosynthesis ; Growth Inhibitors - physiology ; GTP Phosphohydrolases - biosynthesis ; GTP Phosphohydrolases - physiology ; GTP-Binding Proteins - biosynthesis ; GTP-Binding Proteins - physiology ; Immunity, Innate ; Inflammation Mediators - metabolism ; Interferon-beta - biosynthesis ; Interferon-beta - physiology ; Macrophages, Peritoneal - immunology ; Macrophages, Peritoneal - metabolism ; Macrophages, Peritoneal - parasitology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88 - deficiency ; Myeloid Differentiation Factor 88 - genetics ; Receptor, Interferon alpha-beta - deficiency ; Receptor, Interferon alpha-beta - genetics ; Toll-Like Receptors - physiology ; Trypanosoma cruzi ; Trypanosoma cruzi - growth & development ; Trypanosoma cruzi - immunology</subject><ispartof>Journal of Immunology, 2006-11, Vol.177 (10), p.7059-7066</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-66e083ec2945665ef8d65b71128f5b51cd34671d3ab97c02e9640c3eaf475eee3</citedby><cites>FETCH-LOGICAL-c415t-66e083ec2945665ef8d65b71128f5b51cd34671d3ab97c02e9640c3eaf475eee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17082622$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koga, Ritsuko</creatorcontrib><creatorcontrib>Hamano, Shinjiro</creatorcontrib><creatorcontrib>Kuwata, Hirotaka</creatorcontrib><creatorcontrib>Atarashi, Koji</creatorcontrib><creatorcontrib>Ogawa, Masahiro</creatorcontrib><creatorcontrib>Hisaeda, Hajime</creatorcontrib><creatorcontrib>Yamamoto, Masahiro</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Himeno, Kunisuke</creatorcontrib><creatorcontrib>Matsumoto, Makoto</creatorcontrib><creatorcontrib>Takeda, Kiyoshi</creatorcontrib><title>TLR-Dependent Induction of IFN-beta Mediates Host Defense against Trypanosoma cruzi</title><title>Journal of Immunology</title><addtitle>J Immunol</addtitle><description>Host resistance to the intracellular protozoan parasite Trypanosoma cruzi depends on IFN-gamma production by T cells and NK cells. However, the involvement of innate immunity in host resistance to T. cruzi remains unclear. In the present study, we investigated host defense against T. cruzi by focusing on innate immunity. Macrophages and dendritic cells (DCs) from MyD88(-/-)TRIF(-/-) mice, in which TLR-dependent activation of innate immunity was abolished, were defective in the clearance of T. cruzi and showed impaired induction of IFN-beta during T. cruzi infection. Neutralization of IFN-beta in MyD88(-/-) macrophages led to enhanced T. cruzi growth. Cells from MyD88(-/-)IFNAR1(-/-) mice also showed impaired T. cruzi clearance. Furthermore, both MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) mice were highly susceptible to in vivo T. cruzi infection, highlighting the involvement of innate immune responses in T. cruzi infection. We further analyzed the molecular mechanisms for the IFN-beta-mediated antitrypanosomal innate immune responses. MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) macrophages and DCs exhibited defective induction of the GTPase IFN-inducible p47 (IRG47) after T. cruzi infection. RNA interference-mediated reduction of IRG47 expression in MyD88(-/-) macrophages resulted in increased intracellular growth of T. cruzi. These findings suggest that TLR-dependent expression of IFN-beta is involved in resistance to T. cruzi infection through the induction of IRG47.</description><subject>Adaptor Proteins, Vesicular Transport - deficiency</subject><subject>Adaptor Proteins, Vesicular Transport - genetics</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Chagas Disease - genetics</subject><subject>Chagas Disease - immunology</subject><subject>Chagas Disease - parasitology</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - metabolism</subject><subject>Dendritic Cells - parasitology</subject><subject>Gene Expression Regulation - immunology</subject><subject>Growth Inhibitors - biosynthesis</subject><subject>Growth Inhibitors - physiology</subject><subject>GTP Phosphohydrolases - biosynthesis</subject><subject>GTP Phosphohydrolases - physiology</subject><subject>GTP-Binding Proteins - biosynthesis</subject><subject>GTP-Binding Proteins - physiology</subject><subject>Immunity, Innate</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interferon-beta - biosynthesis</subject><subject>Interferon-beta - physiology</subject><subject>Macrophages, Peritoneal - immunology</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Macrophages, Peritoneal - parasitology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myeloid Differentiation Factor 88 - deficiency</subject><subject>Myeloid Differentiation Factor 88 - genetics</subject><subject>Receptor, Interferon alpha-beta - deficiency</subject><subject>Receptor, Interferon alpha-beta - genetics</subject><subject>Toll-Like Receptors - physiology</subject><subject>Trypanosoma cruzi</subject><subject>Trypanosoma cruzi - growth & development</subject><subject>Trypanosoma cruzi - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOwzAQRS0EgvL4A4SyQmxSbMePZIl4ViogQVlbjjNpjRK7xIkq-HpctQh2rEYzOnM1cxA6JXjMMCsu323bDs43YyLlOA4l5sUOGhHOcSoEFrtohDGlKZFCHqDDEN4xxgJTto8OiMQ5FZSO0Ots-pLewBJcBa5PJq4aTG-9S3ydTO6e0hJ6nTxCZXUPIXnwoU9uoAYXINFzbV3sZ93nUjsffKsT0w1f9hjt1boJcLKtR-jt7nZ2_ZBOn-8n11fT1DDC-3gk4DwDQwvGheBQ55XgpSSE5jUvOTFVxoQkVabLQhpMoRAMmwx0zSQHgOwInW9yl53_GCD0qrXBQNNoB34ISuQkvpkV_4KkyAouSB5BtgFN50PooFbLzra6-1QEq7V19WNdRevr4dp6XDvb5g9lC9Xv0lZzBC42wMLOFyvbgQqtbpqIE7Varf5mfQPHhI09</recordid><startdate>20061115</startdate><enddate>20061115</enddate><creator>Koga, Ritsuko</creator><creator>Hamano, Shinjiro</creator><creator>Kuwata, Hirotaka</creator><creator>Atarashi, Koji</creator><creator>Ogawa, Masahiro</creator><creator>Hisaeda, Hajime</creator><creator>Yamamoto, Masahiro</creator><creator>Akira, Shizuo</creator><creator>Himeno, Kunisuke</creator><creator>Matsumoto, Makoto</creator><creator>Takeda, Kiyoshi</creator><general>Am Assoc Immnol</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>7T5</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>20061115</creationdate><title>TLR-Dependent Induction of IFN-beta Mediates Host Defense against Trypanosoma cruzi</title><author>Koga, Ritsuko ; Hamano, Shinjiro ; Kuwata, Hirotaka ; Atarashi, Koji ; Ogawa, Masahiro ; Hisaeda, Hajime ; Yamamoto, Masahiro ; Akira, Shizuo ; Himeno, Kunisuke ; Matsumoto, Makoto ; Takeda, Kiyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-66e083ec2945665ef8d65b71128f5b51cd34671d3ab97c02e9640c3eaf475eee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adaptor Proteins, Vesicular Transport - deficiency</topic><topic>Adaptor Proteins, Vesicular Transport - genetics</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Chagas Disease - genetics</topic><topic>Chagas Disease - immunology</topic><topic>Chagas Disease - parasitology</topic><topic>Dendritic Cells - immunology</topic><topic>Dendritic Cells - metabolism</topic><topic>Dendritic Cells - parasitology</topic><topic>Gene Expression Regulation - immunology</topic><topic>Growth Inhibitors - biosynthesis</topic><topic>Growth Inhibitors - physiology</topic><topic>GTP Phosphohydrolases - biosynthesis</topic><topic>GTP Phosphohydrolases - physiology</topic><topic>GTP-Binding Proteins - biosynthesis</topic><topic>GTP-Binding Proteins - physiology</topic><topic>Immunity, Innate</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interferon-beta - biosynthesis</topic><topic>Interferon-beta - physiology</topic><topic>Macrophages, Peritoneal - immunology</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Macrophages, Peritoneal - parasitology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myeloid Differentiation Factor 88 - deficiency</topic><topic>Myeloid Differentiation Factor 88 - genetics</topic><topic>Receptor, Interferon alpha-beta - deficiency</topic><topic>Receptor, Interferon alpha-beta - genetics</topic><topic>Toll-Like Receptors - physiology</topic><topic>Trypanosoma cruzi</topic><topic>Trypanosoma cruzi - growth & development</topic><topic>Trypanosoma cruzi - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koga, Ritsuko</creatorcontrib><creatorcontrib>Hamano, Shinjiro</creatorcontrib><creatorcontrib>Kuwata, Hirotaka</creatorcontrib><creatorcontrib>Atarashi, Koji</creatorcontrib><creatorcontrib>Ogawa, Masahiro</creatorcontrib><creatorcontrib>Hisaeda, Hajime</creatorcontrib><creatorcontrib>Yamamoto, Masahiro</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Himeno, Kunisuke</creatorcontrib><creatorcontrib>Matsumoto, Makoto</creatorcontrib><creatorcontrib>Takeda, Kiyoshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koga, Ritsuko</au><au>Hamano, Shinjiro</au><au>Kuwata, Hirotaka</au><au>Atarashi, Koji</au><au>Ogawa, Masahiro</au><au>Hisaeda, Hajime</au><au>Yamamoto, Masahiro</au><au>Akira, Shizuo</au><au>Himeno, Kunisuke</au><au>Matsumoto, Makoto</au><au>Takeda, Kiyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR-Dependent Induction of IFN-beta Mediates Host Defense against Trypanosoma cruzi</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2006-11-15</date><risdate>2006</risdate><volume>177</volume><issue>10</issue><spage>7059</spage><epage>7066</epage><pages>7059-7066</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><abstract>Host resistance to the intracellular protozoan parasite Trypanosoma cruzi depends on IFN-gamma production by T cells and NK cells. However, the involvement of innate immunity in host resistance to T. cruzi remains unclear. In the present study, we investigated host defense against T. cruzi by focusing on innate immunity. Macrophages and dendritic cells (DCs) from MyD88(-/-)TRIF(-/-) mice, in which TLR-dependent activation of innate immunity was abolished, were defective in the clearance of T. cruzi and showed impaired induction of IFN-beta during T. cruzi infection. Neutralization of IFN-beta in MyD88(-/-) macrophages led to enhanced T. cruzi growth. Cells from MyD88(-/-)IFNAR1(-/-) mice also showed impaired T. cruzi clearance. Furthermore, both MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) mice were highly susceptible to in vivo T. cruzi infection, highlighting the involvement of innate immune responses in T. cruzi infection. We further analyzed the molecular mechanisms for the IFN-beta-mediated antitrypanosomal innate immune responses. MyD88(-/-)TRIF(-/-) and MyD88(-/-)IFNAR1(-/-) macrophages and DCs exhibited defective induction of the GTPase IFN-inducible p47 (IRG47) after T. cruzi infection. RNA interference-mediated reduction of IRG47 expression in MyD88(-/-) macrophages resulted in increased intracellular growth of T. cruzi. These findings suggest that TLR-dependent expression of IFN-beta is involved in resistance to T. cruzi infection through the induction of IRG47.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>17082622</pmid><doi>10.4049/jimmunol.177.10.7059</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Vesicular Transport - deficiency Adaptor Proteins, Vesicular Transport - genetics Animals Cells, Cultured Chagas Disease - genetics Chagas Disease - immunology Chagas Disease - parasitology Dendritic Cells - immunology Dendritic Cells - metabolism Dendritic Cells - parasitology Gene Expression Regulation - immunology Growth Inhibitors - biosynthesis Growth Inhibitors - physiology GTP Phosphohydrolases - biosynthesis GTP Phosphohydrolases - physiology GTP-Binding Proteins - biosynthesis GTP-Binding Proteins - physiology Immunity, Innate Inflammation Mediators - metabolism Interferon-beta - biosynthesis Interferon-beta - physiology Macrophages, Peritoneal - immunology Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - parasitology Mice Mice, Inbred C57BL Mice, Knockout Myeloid Differentiation Factor 88 - deficiency Myeloid Differentiation Factor 88 - genetics Receptor, Interferon alpha-beta - deficiency Receptor, Interferon alpha-beta - genetics Toll-Like Receptors - physiology Trypanosoma cruzi Trypanosoma cruzi - growth & development Trypanosoma cruzi - immunology |
| title | TLR-Dependent Induction of IFN-beta Mediates Host Defense against Trypanosoma cruzi |
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