Trypanosoma cruzi: parasite shed vesicles increase heart parasitism and generate an intense inflammatory response
Trypanosoma cruzi trypomastigotes continuously shed into the medium plasma membrane fragments sealed as vesicles enriched in glycoproteins of the gp85 and trans-sialidase (TS) superfamily and α-galactosyl-containing glycoconjugates. Injection of a vesicle fraction into BALB/c mice prior to T. cruzi...
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| Veröffentlicht in: | Microbes and infection 2009, Vol.11 (1), p.29-39 |
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| creator | Trocoli Torrecilhas, Ana Claudia Tonelli, Renata Rosito Pavanelli, Wander Rogério da Silva, João Santana Schumacher, Robert Ivan de Souza, Wanderley e Silva, Narcisa Cunha de Almeida Abrahamsohn, Ises Colli, Walter Manso Alves, Maria Júlia |
| description | Trypanosoma cruzi trypomastigotes continuously shed into the medium plasma membrane fragments sealed as vesicles enriched in glycoproteins of the gp85 and trans-sialidase (TS) superfamily and α-galactosyl-containing glycoconjugates. Injection of a vesicle fraction into BALB/c mice prior to
T. cruzi infection led to 40% of deaths on the 16th
day post-infection and 100% on day 20th whereas 20% of untreated animals survived for more than 30
days. The vesicle-treated animals developed severe heart pathology, with intense inflammatory reaction and higher number of amastigote nests. Analysis of the inflammatory infiltrates 15
days after infection showed predominance of TCD4
+ lymphocytes and macrophages, but not of TCD8
+ cells, as well as a decrease of areas labeled with anti-iNOS antibodies as compared to the control. Higher levels of IL-4 and IL-10 mRNAs were found in the hearts and higher IL-10 and lower NO levels in splenocytes of vesicles pretreated animals. Treatment of mice with neutralizing anti-IL-10 or anti-IL-4 antibodies precluded the effects of pre-inoculation of membrane vesicles on infection. These results indicate that
T. cruzi shed membrane components increase tissue parasitism and inflammation by stimulation of IL-4 and IL-10 synthesis and thus may play a central role in the pathogenesis of Chagas’ disease acute phase. |
| doi_str_mv | 10.1016/j.micinf.2008.10.003 |
| format | Article |
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T. cruzi infection led to 40% of deaths on the 16th
day post-infection and 100% on day 20th whereas 20% of untreated animals survived for more than 30
days. The vesicle-treated animals developed severe heart pathology, with intense inflammatory reaction and higher number of amastigote nests. Analysis of the inflammatory infiltrates 15
days after infection showed predominance of TCD4
+ lymphocytes and macrophages, but not of TCD8
+ cells, as well as a decrease of areas labeled with anti-iNOS antibodies as compared to the control. Higher levels of IL-4 and IL-10 mRNAs were found in the hearts and higher IL-10 and lower NO levels in splenocytes of vesicles pretreated animals. Treatment of mice with neutralizing anti-IL-10 or anti-IL-4 antibodies precluded the effects of pre-inoculation of membrane vesicles on infection. These results indicate that
T. cruzi shed membrane components increase tissue parasitism and inflammation by stimulation of IL-4 and IL-10 synthesis and thus may play a central role in the pathogenesis of Chagas’ disease acute phase.</description><identifier>ISSN: 1286-4579</identifier><identifier>EISSN: 1769-714X</identifier><identifier>DOI: 10.1016/j.micinf.2008.10.003</identifier><identifier>PMID: 19028594</identifier><language>eng</language><publisher>Kidlington: Elsevier SAS</publisher><subject>Animals ; Biological and medical sciences ; CD4-Positive T-Lymphocytes - immunology ; Cell Membrane - chemistry ; Cell Membrane - immunology ; Chagas Cardiomyopathy - immunology ; Chagas Cardiomyopathy - mortality ; Chagas Cardiomyopathy - parasitology ; Chagas Cardiomyopathy - physiopathology ; Cytokines ; Female ; Fundamental and applied biological sciences. Psychology ; Glycoproteins - analysis ; Heart - parasitology ; Inflammation - immunology ; Inflammation - parasitology ; Inflammation - physiopathology ; Interleukin-10 - biosynthesis ; Interleukin-4 - biosynthesis ; Life cycle. Host-agent relationship. Pathogenesis ; Macrophages - immunology ; Mice ; Mice, Inbred BALB C ; Microbiology ; Myocardium - immunology ; Myocardium - pathology ; Neuraminidase - analysis ; Protozoa ; T. cruzi infectivity ; Tissue parasitism ; Trypanosoma cruzi - immunology ; Trypanosoma cruzi - pathogenicity ; Virulence</subject><ispartof>Microbes and infection, 2009, Vol.11 (1), p.29-39</ispartof><rights>2008 Elsevier Masson SAS</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-163c615f3e8c935b8eca7f7a1209f1b1f756f917ea3bb3b42518dd6cf76c9a963</citedby><cites>FETCH-LOGICAL-c456t-163c615f3e8c935b8eca7f7a1209f1b1f756f917ea3bb3b42518dd6cf76c9a963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.micinf.2008.10.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,4025,27928,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21138739$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19028594$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Trocoli Torrecilhas, Ana Claudia</creatorcontrib><creatorcontrib>Tonelli, Renata Rosito</creatorcontrib><creatorcontrib>Pavanelli, Wander Rogério</creatorcontrib><creatorcontrib>da Silva, João Santana</creatorcontrib><creatorcontrib>Schumacher, Robert Ivan</creatorcontrib><creatorcontrib>de Souza, Wanderley</creatorcontrib><creatorcontrib>e Silva, Narcisa Cunha</creatorcontrib><creatorcontrib>de Almeida Abrahamsohn, Ises</creatorcontrib><creatorcontrib>Colli, Walter</creatorcontrib><creatorcontrib>Manso Alves, Maria Júlia</creatorcontrib><title>Trypanosoma cruzi: parasite shed vesicles increase heart parasitism and generate an intense inflammatory response</title><title>Microbes and infection</title><addtitle>Microbes Infect</addtitle><description>Trypanosoma cruzi trypomastigotes continuously shed into the medium plasma membrane fragments sealed as vesicles enriched in glycoproteins of the gp85 and trans-sialidase (TS) superfamily and α-galactosyl-containing glycoconjugates. Injection of a vesicle fraction into BALB/c mice prior to
T. cruzi infection led to 40% of deaths on the 16th
day post-infection and 100% on day 20th whereas 20% of untreated animals survived for more than 30
days. The vesicle-treated animals developed severe heart pathology, with intense inflammatory reaction and higher number of amastigote nests. Analysis of the inflammatory infiltrates 15
days after infection showed predominance of TCD4
+ lymphocytes and macrophages, but not of TCD8
+ cells, as well as a decrease of areas labeled with anti-iNOS antibodies as compared to the control. Higher levels of IL-4 and IL-10 mRNAs were found in the hearts and higher IL-10 and lower NO levels in splenocytes of vesicles pretreated animals. Treatment of mice with neutralizing anti-IL-10 or anti-IL-4 antibodies precluded the effects of pre-inoculation of membrane vesicles on infection. These results indicate that
T. cruzi shed membrane components increase tissue parasitism and inflammation by stimulation of IL-4 and IL-10 synthesis and thus may play a central role in the pathogenesis of Chagas’ disease acute phase.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Cell Membrane - chemistry</subject><subject>Cell Membrane - immunology</subject><subject>Chagas Cardiomyopathy - immunology</subject><subject>Chagas Cardiomyopathy - mortality</subject><subject>Chagas Cardiomyopathy - parasitology</subject><subject>Chagas Cardiomyopathy - physiopathology</subject><subject>Cytokines</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycoproteins - analysis</subject><subject>Heart - parasitology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - parasitology</subject><subject>Inflammation - physiopathology</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Life cycle. Host-agent relationship. Pathogenesis</subject><subject>Macrophages - immunology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microbiology</subject><subject>Myocardium - immunology</subject><subject>Myocardium - pathology</subject><subject>Neuraminidase - analysis</subject><subject>Protozoa</subject><subject>T. cruzi infectivity</subject><subject>Tissue parasitism</subject><subject>Trypanosoma cruzi - immunology</subject><subject>Trypanosoma cruzi - pathogenicity</subject><subject>Virulence</subject><issn>1286-4579</issn><issn>1769-714X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1r3DAQhk1paNK0_6AUXZqbt5Jl66OHQgnpBwR6SaE3MZZHjRZbdjTewPbXR8tu21tPM7w87zA8VfVG8I3gQr3fbqboYwqbhnNTog3n8ll1IbSytRbtz-dlb4yq207b8-ol0ZZz0WnVvqjOheWN6Wx7UT3c5f0CaaZ5Aubz7nf8wBbIQHFFRvc4sEek6EckFpPPCITsHiGvf6hIE4M0sF-YMEMpQSrkiqmA5bsRpgnWOe9ZRlrmkr6qzgKMhK9P87L68fnm7vprffv9y7frT7e1bzu11kJJr0QXJBpvZdcb9KCDBtFwG0Qvgu5UsEIjyL6Xfdt0wgyD8kErb8EqeVldHe8ueX7YIa1uiuRxHCHhvCOnlGmLA1PA9gj6PBNlDG7JcYK8d4K7g2q3dUfV7qD6kBbVpfb2dH_XTzj8K53cFuDdCQDyMIYMyUf6yzVCSKOlLdzHI4fFxmPE7MhHTB6HmNGvbpjj_z95ArgvoXU</recordid><startdate>2009</startdate><enddate>2009</enddate><creator>Trocoli Torrecilhas, Ana Claudia</creator><creator>Tonelli, Renata Rosito</creator><creator>Pavanelli, Wander Rogério</creator><creator>da Silva, João Santana</creator><creator>Schumacher, Robert Ivan</creator><creator>de Souza, Wanderley</creator><creator>e Silva, Narcisa Cunha</creator><creator>de Almeida Abrahamsohn, Ises</creator><creator>Colli, Walter</creator><creator>Manso Alves, Maria Júlia</creator><general>Elsevier SAS</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>2009</creationdate><title>Trypanosoma cruzi: parasite shed vesicles increase heart parasitism and generate an intense inflammatory response</title><author>Trocoli Torrecilhas, Ana Claudia ; Tonelli, Renata Rosito ; Pavanelli, Wander Rogério ; da Silva, João Santana ; Schumacher, Robert Ivan ; de Souza, Wanderley ; e Silva, Narcisa Cunha ; de Almeida Abrahamsohn, Ises ; Colli, Walter ; Manso Alves, Maria Júlia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-163c615f3e8c935b8eca7f7a1209f1b1f756f917ea3bb3b42518dd6cf76c9a963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Cell Membrane - chemistry</topic><topic>Cell Membrane - immunology</topic><topic>Chagas Cardiomyopathy - immunology</topic><topic>Chagas Cardiomyopathy - mortality</topic><topic>Chagas Cardiomyopathy - parasitology</topic><topic>Chagas Cardiomyopathy - physiopathology</topic><topic>Cytokines</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycoproteins - analysis</topic><topic>Heart - parasitology</topic><topic>Inflammation - immunology</topic><topic>Inflammation - parasitology</topic><topic>Inflammation - physiopathology</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Life cycle. Host-agent relationship. Pathogenesis</topic><topic>Macrophages - immunology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Microbiology</topic><topic>Myocardium - immunology</topic><topic>Myocardium - pathology</topic><topic>Neuraminidase - analysis</topic><topic>Protozoa</topic><topic>T. cruzi infectivity</topic><topic>Tissue parasitism</topic><topic>Trypanosoma cruzi - immunology</topic><topic>Trypanosoma cruzi - pathogenicity</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Trocoli Torrecilhas, Ana Claudia</creatorcontrib><creatorcontrib>Tonelli, Renata Rosito</creatorcontrib><creatorcontrib>Pavanelli, Wander Rogério</creatorcontrib><creatorcontrib>da Silva, João Santana</creatorcontrib><creatorcontrib>Schumacher, Robert Ivan</creatorcontrib><creatorcontrib>de Souza, Wanderley</creatorcontrib><creatorcontrib>e Silva, Narcisa Cunha</creatorcontrib><creatorcontrib>de Almeida Abrahamsohn, Ises</creatorcontrib><creatorcontrib>Colli, Walter</creatorcontrib><creatorcontrib>Manso Alves, Maria Júlia</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>MEDLINE - Academic</collection><jtitle>Microbes and infection</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Trocoli Torrecilhas, Ana Claudia</au><au>Tonelli, Renata Rosito</au><au>Pavanelli, Wander Rogério</au><au>da Silva, João Santana</au><au>Schumacher, Robert Ivan</au><au>de Souza, Wanderley</au><au>e Silva, Narcisa Cunha</au><au>de Almeida Abrahamsohn, Ises</au><au>Colli, Walter</au><au>Manso Alves, Maria Júlia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Trypanosoma cruzi: parasite shed vesicles increase heart parasitism and generate an intense inflammatory response</atitle><jtitle>Microbes and infection</jtitle><addtitle>Microbes Infect</addtitle><date>2009</date><risdate>2009</risdate><volume>11</volume><issue>1</issue><spage>29</spage><epage>39</epage><pages>29-39</pages><issn>1286-4579</issn><eissn>1769-714X</eissn><abstract>Trypanosoma cruzi trypomastigotes continuously shed into the medium plasma membrane fragments sealed as vesicles enriched in glycoproteins of the gp85 and trans-sialidase (TS) superfamily and α-galactosyl-containing glycoconjugates. Injection of a vesicle fraction into BALB/c mice prior to
T. cruzi infection led to 40% of deaths on the 16th
day post-infection and 100% on day 20th whereas 20% of untreated animals survived for more than 30
days. The vesicle-treated animals developed severe heart pathology, with intense inflammatory reaction and higher number of amastigote nests. Analysis of the inflammatory infiltrates 15
days after infection showed predominance of TCD4
+ lymphocytes and macrophages, but not of TCD8
+ cells, as well as a decrease of areas labeled with anti-iNOS antibodies as compared to the control. Higher levels of IL-4 and IL-10 mRNAs were found in the hearts and higher IL-10 and lower NO levels in splenocytes of vesicles pretreated animals. Treatment of mice with neutralizing anti-IL-10 or anti-IL-4 antibodies precluded the effects of pre-inoculation of membrane vesicles on infection. These results indicate that
T. cruzi shed membrane components increase tissue parasitism and inflammation by stimulation of IL-4 and IL-10 synthesis and thus may play a central role in the pathogenesis of Chagas’ disease acute phase.</abstract><cop>Kidlington</cop><pub>Elsevier SAS</pub><pmid>19028594</pmid><doi>10.1016/j.micinf.2008.10.003</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1286-4579 |
| ispartof | Microbes and infection, 2009, Vol.11 (1), p.29-39 |
| issn | 1286-4579 1769-714X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_66848598 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Biological and medical sciences CD4-Positive T-Lymphocytes - immunology Cell Membrane - chemistry Cell Membrane - immunology Chagas Cardiomyopathy - immunology Chagas Cardiomyopathy - mortality Chagas Cardiomyopathy - parasitology Chagas Cardiomyopathy - physiopathology Cytokines Female Fundamental and applied biological sciences. Psychology Glycoproteins - analysis Heart - parasitology Inflammation - immunology Inflammation - parasitology Inflammation - physiopathology Interleukin-10 - biosynthesis Interleukin-4 - biosynthesis Life cycle. Host-agent relationship. Pathogenesis Macrophages - immunology Mice Mice, Inbred BALB C Microbiology Myocardium - immunology Myocardium - pathology Neuraminidase - analysis Protozoa T. cruzi infectivity Tissue parasitism Trypanosoma cruzi - immunology Trypanosoma cruzi - pathogenicity Virulence |
| title | Trypanosoma cruzi: parasite shed vesicles increase heart parasitism and generate an intense inflammatory response |
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