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Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii
We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha) in the dually infected mice suggested a role for t...
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Published in: | Infection and immunity 2001-03, Vol.69 (3), p.1454-1462 |
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description | We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12(-/-) (IL-12(-/-)) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12(-/-) mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-alpha, gamma interferon, and NO produced by splenocytes from coinfected IL-12(-/-) mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12(-/-) mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-alpha are implicated in this process. |
doi_str_mv | 10.1128/IAI.69.3.1454-1462.2001 |
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M.</contributor><creatorcontrib>ARAUJO, Maria Ilma ; BLISS, Susan K ; SUZUKI, Yasuhiro ; ALCARAZ, Ana ; DENKERS, Eric Y ; PEARCE, Edward J ; Mansfield, J. M.</creatorcontrib><description>We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12(-/-) (IL-12(-/-)) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12(-/-) mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-alpha, gamma interferon, and NO produced by splenocytes from coinfected IL-12(-/-) mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12(-/-) mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-alpha are implicated in this process.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.69.3.1454-1462.2001</identifier><identifier>PMID: 11179312</identifier><identifier>CODEN: INFIBR</identifier><language>eng</language><publisher>Washington, DC: American Society for Microbiology</publisher><subject>Animals ; Bacterial diseases ; Biological and medical sciences ; Experimental bacterial diseases and models ; Experimental helminthic diseases. Models ; Female ; Fundamental and applied biological sciences. Psychology ; Fungal and Parasitic Infections ; Helminthic diseases ; Infectious diseases ; Inflammation Mediators - metabolism ; Interleukin-12 - genetics ; Interleukin-12 - immunology ; Liver - pathology ; Medical sciences ; Mice ; Mice, Mutant Strains ; Microbiology ; Parasitic diseases ; Schistosoma mansoni ; Schistosomiasis mansoni - complications ; Schistosomiasis mansoni - immunology ; Schistosomiasis mansoni - mortality ; Schistosomiasis mansoni - pathology ; Survival Analysis ; Survivors ; Th2 Cells ; Toxoplasma gondii ; Toxoplasmosis, Animal - complications ; Toxoplasmosis, Animal - immunology ; Toxoplasmosis, Animal - mortality ; Toxoplasmosis, Animal - pathology</subject><ispartof>Infection and immunity, 2001-03, Vol.69 (3), p.1454-1462</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright © 2001, American Society for Microbiology 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-9f57d7a6c711cdccd2b8e127379cbc73cfa30dfd3aa6bc66243ca43f616678363</citedby><cites>FETCH-LOGICAL-c423t-9f57d7a6c711cdccd2b8e127379cbc73cfa30dfd3aa6bc66243ca43f616678363</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/PMC98041/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC98041/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3188,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14160480$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11179312$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mansfield, J. M.</contributor><creatorcontrib>ARAUJO, Maria Ilma</creatorcontrib><creatorcontrib>BLISS, Susan K</creatorcontrib><creatorcontrib>SUZUKI, Yasuhiro</creatorcontrib><creatorcontrib>ALCARAZ, Ana</creatorcontrib><creatorcontrib>DENKERS, Eric Y</creatorcontrib><creatorcontrib>PEARCE, Edward J</creatorcontrib><title>Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii</title><title>Infection and immunity</title><addtitle>Infect Immun</addtitle><description>We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12(-/-) (IL-12(-/-)) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12(-/-) mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-alpha, gamma interferon, and NO produced by splenocytes from coinfected IL-12(-/-) mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12(-/-) mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-alpha are implicated in this process.</description><subject>Animals</subject><subject>Bacterial diseases</subject><subject>Biological and medical sciences</subject><subject>Experimental bacterial diseases and models</subject><subject>Experimental helminthic diseases. Models</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fungal and Parasitic Infections</subject><subject>Helminthic diseases</subject><subject>Infectious diseases</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-12 - genetics</subject><subject>Interleukin-12 - immunology</subject><subject>Liver - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Microbiology</subject><subject>Parasitic diseases</subject><subject>Schistosoma mansoni</subject><subject>Schistosomiasis mansoni - complications</subject><subject>Schistosomiasis mansoni - immunology</subject><subject>Schistosomiasis mansoni - mortality</subject><subject>Schistosomiasis mansoni - pathology</subject><subject>Survival Analysis</subject><subject>Survivors</subject><subject>Th2 Cells</subject><subject>Toxoplasma gondii</subject><subject>Toxoplasmosis, Animal - complications</subject><subject>Toxoplasmosis, Animal - immunology</subject><subject>Toxoplasmosis, Animal - mortality</subject><subject>Toxoplasmosis, Animal - pathology</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNqFkc2OFCEURonROO3oKygb3VXJBQqqEjeTiT-dTOLCcU3oC9WNVkEL1TOa-PDSTsfRlSvC_c5HLjmEvADWAvD-9fpi3aqhFS3ITjYgFW85Y_CArIANfdN1nD8kqzoZmqFT-ow8KeVLvUop-8fkDAD0IICvyM91XHye_OFriA1wus9pTosvdG-XXZrSNiCdwo3PFHc2bmtgo6PO15SGSOeAnmIKcfS4eEdvQ51_wl0oSypptnS2saQYfreu0_e0n2yp422KLoSn5NFop-Kfnc5z8vnd2-vLD83Vx_fry4urBiUXSzOMnXbaKtQA6BAd3_QeuBZ6wA1qgaMVzI1OWKs2qBSXAq0UowKldC-UOCdv7t7dHzazd-jjku1k9jnMNv8wyQbzbxLDzmzTjRl6JqHWX53qOX07-LKYORT002SjT4diNFMCoGf_BUH3Xdd3soL6DsScSsl-_LMLMHMUbKpgowYjzFGwOQo2R8G1-fzvr9z3TkYr8PIE2IJ2GrONGMo9J0ExWXf9BVuJsok</recordid><startdate>20010301</startdate><enddate>20010301</enddate><creator>ARAUJO, Maria Ilma</creator><creator>BLISS, Susan K</creator><creator>SUZUKI, Yasuhiro</creator><creator>ALCARAZ, Ana</creator><creator>DENKERS, Eric Y</creator><creator>PEARCE, Edward J</creator><general>American Society for Microbiology</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>7T5</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20010301</creationdate><title>Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii</title><author>ARAUJO, Maria Ilma ; BLISS, Susan K ; SUZUKI, Yasuhiro ; ALCARAZ, Ana ; DENKERS, Eric Y ; PEARCE, Edward J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-9f57d7a6c711cdccd2b8e127379cbc73cfa30dfd3aa6bc66243ca43f616678363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Bacterial diseases</topic><topic>Biological and medical sciences</topic><topic>Experimental bacterial diseases and models</topic><topic>Experimental helminthic diseases. Models</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fungal and Parasitic Infections</topic><topic>Helminthic diseases</topic><topic>Infectious diseases</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-12 - genetics</topic><topic>Interleukin-12 - immunology</topic><topic>Liver - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Microbiology</topic><topic>Parasitic diseases</topic><topic>Schistosoma mansoni</topic><topic>Schistosomiasis mansoni - complications</topic><topic>Schistosomiasis mansoni - immunology</topic><topic>Schistosomiasis mansoni - mortality</topic><topic>Schistosomiasis mansoni - pathology</topic><topic>Survival Analysis</topic><topic>Survivors</topic><topic>Th2 Cells</topic><topic>Toxoplasma gondii</topic><topic>Toxoplasmosis, Animal - complications</topic><topic>Toxoplasmosis, Animal - immunology</topic><topic>Toxoplasmosis, Animal - mortality</topic><topic>Toxoplasmosis, Animal - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ARAUJO, Maria Ilma</creatorcontrib><creatorcontrib>BLISS, Susan K</creatorcontrib><creatorcontrib>SUZUKI, Yasuhiro</creatorcontrib><creatorcontrib>ALCARAZ, Ana</creatorcontrib><creatorcontrib>DENKERS, Eric Y</creatorcontrib><creatorcontrib>PEARCE, Edward J</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Infection and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ARAUJO, Maria Ilma</au><au>BLISS, Susan K</au><au>SUZUKI, Yasuhiro</au><au>ALCARAZ, Ana</au><au>DENKERS, Eric Y</au><au>PEARCE, Edward J</au><au>Mansfield, J. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii</atitle><jtitle>Infection and immunity</jtitle><addtitle>Infect Immun</addtitle><date>2001-03-01</date><risdate>2001</risdate><volume>69</volume><issue>3</issue><spage>1454</spage><epage>1462</epage><pages>1454-1462</pages><issn>0019-9567</issn><eissn>1098-5522</eissn><coden>INFIBR</coden><abstract>We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12(-/-) (IL-12(-/-)) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12(-/-) mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-alpha, gamma interferon, and NO produced by splenocytes from coinfected IL-12(-/-) mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12(-/-) mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-alpha are implicated in this process.</abstract><cop>Washington, DC</cop><pub>American Society for Microbiology</pub><pmid>11179312</pmid><doi>10.1128/IAI.69.3.1454-1462.2001</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bacterial diseases Biological and medical sciences Experimental bacterial diseases and models Experimental helminthic diseases. Models Female Fundamental and applied biological sciences. Psychology Fungal and Parasitic Infections Helminthic diseases Infectious diseases Inflammation Mediators - metabolism Interleukin-12 - genetics Interleukin-12 - immunology Liver - pathology Medical sciences Mice Mice, Mutant Strains Microbiology Parasitic diseases Schistosoma mansoni Schistosomiasis mansoni - complications Schistosomiasis mansoni - immunology Schistosomiasis mansoni - mortality Schistosomiasis mansoni - pathology Survival Analysis Survivors Th2 Cells Toxoplasma gondii Toxoplasmosis, Animal - complications Toxoplasmosis, Animal - immunology Toxoplasmosis, Animal - mortality Toxoplasmosis, Animal - pathology |
title | Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii |
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