TLR2, TLR4 and TLR9 are differentially modulated in liver lethally injured from BALB/c and C57BL/6 mice during Trypanosoma cruzi acute infection
Toll-like receptor (TLR) family is crucial for microbial elimination and homeostasis, and has an important immunoregulatory role. In this study, we comparatively analyze innate immune response and tissular injury elicited in BALB/c and C57BL/6 (B6) mice during acute Trypanosoma cruzi infection. The...
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| Veröffentlicht in: | Molecular immunology 2008-08, Vol.45 (13), p.3580-3588 |
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| creator | Carrera-Silva, Eugenio Antonio Carolina, Cano Roxana Natalia, Guiñazu Pilar, Aoki Maria Andrea, Pellegrini Gea, Susana |
| description | Toll-like receptor (TLR) family is crucial for microbial elimination and homeostasis, and has an important immunoregulatory role. In this study, we comparatively analyze innate immune response and tissular injury elicited in BALB/c and C57BL/6 (B6) mice during acute
Trypanosoma cruzi infection. The liver was the most affected tissue with numerous cellular infiltrates, apoptotic cells and necrotic areas. The apoptotic rate, evaluated by Hoescht stain, was highest in liver of B6. Infection increased transaminase activities in both mouse strains, although they were highest in B6. BALB/c showed sixfold higher parasitemias than B6 but the latter presented higher mortality (80%) than BALB/c (40%). To gain insight into the molecular basis, we investigated the TLRs commitment in liver. We found that, TLR2 and TLR4 were up-regulated in BALB/c while they were down-regulated in B6. However, TLR9 showed a diminution in BALB/c and an increase in B6 at the end of infection. Moreover, an intensified pro-inflammatory cytokine profile was observed in B6 and F4/80+ and Gr1+ leukocytes were the predominant cells in liver from both mouse strains. Thus, altered TLR2, TLR4 and TLR9 signalling and exacerbate inflammatory cytokine profile could be responsible of the fatal hepatic damage observed in infected B6. |
| doi_str_mv | 10.1016/j.molimm.2008.05.004 |
| format | Article |
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Trypanosoma cruzi infection. The liver was the most affected tissue with numerous cellular infiltrates, apoptotic cells and necrotic areas. The apoptotic rate, evaluated by Hoescht stain, was highest in liver of B6. Infection increased transaminase activities in both mouse strains, although they were highest in B6. BALB/c showed sixfold higher parasitemias than B6 but the latter presented higher mortality (80%) than BALB/c (40%). To gain insight into the molecular basis, we investigated the TLRs commitment in liver. We found that, TLR2 and TLR4 were up-regulated in BALB/c while they were down-regulated in B6. However, TLR9 showed a diminution in BALB/c and an increase in B6 at the end of infection. Moreover, an intensified pro-inflammatory cytokine profile was observed in B6 and F4/80+ and Gr1+ leukocytes were the predominant cells in liver from both mouse strains. Thus, altered TLR2, TLR4 and TLR9 signalling and exacerbate inflammatory cytokine profile could be responsible of the fatal hepatic damage observed in infected B6.</description><identifier>ISSN: 0161-5890</identifier><identifier>EISSN: 1872-9142</identifier><identifier>DOI: 10.1016/j.molimm.2008.05.004</identifier><identifier>PMID: 18565585</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Chagas Disease - genetics ; Chagas Disease - mortality ; Chagas Disease - parasitology ; Chagas Disease - pathology ; Female ; Gene Expression Regulation ; Heart - parasitology ; Hepatic injury ; Inflammation ; Inflammation Mediators - metabolism ; Liver - metabolism ; Liver - parasitology ; Liver - pathology ; Mice ; Mice, Inbred BALB C - genetics ; Mice, Inbred BALB C - metabolism ; Mice, Inbred BALB C - parasitology ; Mice, Inbred C57BL - genetics ; Mice, Inbred C57BL - metabolism ; Mice, Inbred C57BL - parasitology ; Myocardium - metabolism ; Myocardium - pathology ; Parasite infection ; Signal Transduction - genetics ; Spleen - metabolism ; Spleen - pathology ; Survival Analysis ; Toll-like receptor ; Toll-Like Receptor 2 - genetics ; Toll-Like Receptor 2 - metabolism ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism ; Toll-Like Receptor 9 - genetics ; Toll-Like Receptor 9 - metabolism ; Trypanosoma cruzi ; Trypanosoma cruzi - immunology</subject><ispartof>Molecular immunology, 2008-08, Vol.45 (13), p.3580-3588</ispartof><rights>2008 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-e1350fd4522f55ddc91a018c49d7bd889e1d9b98b1067b9939ab0ec0f6c106853</citedby><cites>FETCH-LOGICAL-c423t-e1350fd4522f55ddc91a018c49d7bd889e1d9b98b1067b9939ab0ec0f6c106853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.molimm.2008.05.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3552,27931,27932,46002</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18565585$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Carrera-Silva, Eugenio Antonio</creatorcontrib><creatorcontrib>Carolina, Cano Roxana</creatorcontrib><creatorcontrib>Natalia, Guiñazu</creatorcontrib><creatorcontrib>Pilar, Aoki Maria</creatorcontrib><creatorcontrib>Andrea, Pellegrini</creatorcontrib><creatorcontrib>Gea, Susana</creatorcontrib><title>TLR2, TLR4 and TLR9 are differentially modulated in liver lethally injured from BALB/c and C57BL/6 mice during Trypanosoma cruzi acute infection</title><title>Molecular immunology</title><addtitle>Mol Immunol</addtitle><description>Toll-like receptor (TLR) family is crucial for microbial elimination and homeostasis, and has an important immunoregulatory role. In this study, we comparatively analyze innate immune response and tissular injury elicited in BALB/c and C57BL/6 (B6) mice during acute
Trypanosoma cruzi infection. The liver was the most affected tissue with numerous cellular infiltrates, apoptotic cells and necrotic areas. The apoptotic rate, evaluated by Hoescht stain, was highest in liver of B6. Infection increased transaminase activities in both mouse strains, although they were highest in B6. BALB/c showed sixfold higher parasitemias than B6 but the latter presented higher mortality (80%) than BALB/c (40%). To gain insight into the molecular basis, we investigated the TLRs commitment in liver. We found that, TLR2 and TLR4 were up-regulated in BALB/c while they were down-regulated in B6. However, TLR9 showed a diminution in BALB/c and an increase in B6 at the end of infection. Moreover, an intensified pro-inflammatory cytokine profile was observed in B6 and F4/80+ and Gr1+ leukocytes were the predominant cells in liver from both mouse strains. Thus, altered TLR2, TLR4 and TLR9 signalling and exacerbate inflammatory cytokine profile could be responsible of the fatal hepatic damage observed in infected B6.</description><subject>Animals</subject><subject>Chagas Disease - genetics</subject><subject>Chagas Disease - mortality</subject><subject>Chagas Disease - parasitology</subject><subject>Chagas Disease - pathology</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Heart - parasitology</subject><subject>Hepatic injury</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Liver - metabolism</subject><subject>Liver - parasitology</subject><subject>Liver - pathology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C - genetics</subject><subject>Mice, Inbred BALB C - metabolism</subject><subject>Mice, Inbred BALB C - parasitology</subject><subject>Mice, Inbred C57BL - genetics</subject><subject>Mice, Inbred C57BL - metabolism</subject><subject>Mice, Inbred C57BL - parasitology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Parasite infection</subject><subject>Signal Transduction - genetics</subject><subject>Spleen - metabolism</subject><subject>Spleen - pathology</subject><subject>Survival Analysis</subject><subject>Toll-like receptor</subject><subject>Toll-Like Receptor 2 - genetics</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-Like Receptor 9 - genetics</subject><subject>Toll-Like Receptor 9 - metabolism</subject><subject>Trypanosoma cruzi</subject><subject>Trypanosoma cruzi - immunology</subject><issn>0161-5890</issn><issn>1872-9142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc-K2zAQxkVp6Wa3fYNSdOpe1o5kW7J0KWxC_4GhUNKzkKVxq2BZqWQvpE_RR66yCfS2vYwGzW--ge9D6A0lJSWUr_elD6PzvqwIESVhJSHNM7Sioq0KSZvqOVpljBZMSHKFrlPaE0I44ewluqKCccYEW6E_u-5bdYdzbbCe7KmRWEfA1g0DRJhmp8fxiH2wy6hnsNhNeHQPEPEI88_HmZv2S8yTIQaPN_fdZm0etbas3XRrjr0zWW-JbvqBd_F40FNIwWts4vLbYW2WGbLGAGZ2YXqFXgx6TPD68t6g7x8_7Lafi-7rpy_b-64wTVXPBdCakcE2rKoGxqw1kmpChWmkbXsrhARqZS9FTwlveylrqXsChgzc5B_B6ht0e9Y9xPBrgTQr75KBcdQThCUpIWpSy5afyHdPklzWNBva_BekkgspqcxgcwZNDClFGNQhOq_jUVGiTuGqvTqHq07hKsJUDjevvb3oL70H-2_pkmYG3p8ByMY9OIgqGQeTAetidlfZ4J6-8Be0ELZp</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Carrera-Silva, Eugenio Antonio</creator><creator>Carolina, Cano Roxana</creator><creator>Natalia, Guiñazu</creator><creator>Pilar, Aoki Maria</creator><creator>Andrea, Pellegrini</creator><creator>Gea, Susana</creator><general>Elsevier Ltd</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>20080801</creationdate><title>TLR2, TLR4 and TLR9 are differentially modulated in liver lethally injured from BALB/c and C57BL/6 mice during Trypanosoma cruzi acute infection</title><author>Carrera-Silva, Eugenio Antonio ; Carolina, Cano Roxana ; Natalia, Guiñazu ; Pilar, Aoki Maria ; Andrea, Pellegrini ; Gea, Susana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-e1350fd4522f55ddc91a018c49d7bd889e1d9b98b1067b9939ab0ec0f6c106853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Chagas Disease - genetics</topic><topic>Chagas Disease - mortality</topic><topic>Chagas Disease - parasitology</topic><topic>Chagas Disease - pathology</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Heart - parasitology</topic><topic>Hepatic injury</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Liver - metabolism</topic><topic>Liver - parasitology</topic><topic>Liver - pathology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C - genetics</topic><topic>Mice, Inbred BALB C - metabolism</topic><topic>Mice, Inbred BALB C - parasitology</topic><topic>Mice, Inbred C57BL - genetics</topic><topic>Mice, Inbred C57BL - metabolism</topic><topic>Mice, Inbred C57BL - parasitology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Parasite infection</topic><topic>Signal Transduction - genetics</topic><topic>Spleen - metabolism</topic><topic>Spleen - pathology</topic><topic>Survival Analysis</topic><topic>Toll-like receptor</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Toll-Like Receptor 9 - genetics</topic><topic>Toll-Like Receptor 9 - metabolism</topic><topic>Trypanosoma cruzi</topic><topic>Trypanosoma cruzi - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carrera-Silva, Eugenio Antonio</creatorcontrib><creatorcontrib>Carolina, Cano Roxana</creatorcontrib><creatorcontrib>Natalia, Guiñazu</creatorcontrib><creatorcontrib>Pilar, Aoki Maria</creatorcontrib><creatorcontrib>Andrea, Pellegrini</creatorcontrib><creatorcontrib>Gea, Susana</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>Molecular immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carrera-Silva, Eugenio Antonio</au><au>Carolina, Cano Roxana</au><au>Natalia, Guiñazu</au><au>Pilar, Aoki Maria</au><au>Andrea, Pellegrini</au><au>Gea, Susana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR2, TLR4 and TLR9 are differentially modulated in liver lethally injured from BALB/c and C57BL/6 mice during Trypanosoma cruzi acute infection</atitle><jtitle>Molecular immunology</jtitle><addtitle>Mol Immunol</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>45</volume><issue>13</issue><spage>3580</spage><epage>3588</epage><pages>3580-3588</pages><issn>0161-5890</issn><eissn>1872-9142</eissn><abstract>Toll-like receptor (TLR) family is crucial for microbial elimination and homeostasis, and has an important immunoregulatory role. In this study, we comparatively analyze innate immune response and tissular injury elicited in BALB/c and C57BL/6 (B6) mice during acute
Trypanosoma cruzi infection. The liver was the most affected tissue with numerous cellular infiltrates, apoptotic cells and necrotic areas. The apoptotic rate, evaluated by Hoescht stain, was highest in liver of B6. Infection increased transaminase activities in both mouse strains, although they were highest in B6. BALB/c showed sixfold higher parasitemias than B6 but the latter presented higher mortality (80%) than BALB/c (40%). To gain insight into the molecular basis, we investigated the TLRs commitment in liver. We found that, TLR2 and TLR4 were up-regulated in BALB/c while they were down-regulated in B6. However, TLR9 showed a diminution in BALB/c and an increase in B6 at the end of infection. Moreover, an intensified pro-inflammatory cytokine profile was observed in B6 and F4/80+ and Gr1+ leukocytes were the predominant cells in liver from both mouse strains. Thus, altered TLR2, TLR4 and TLR9 signalling and exacerbate inflammatory cytokine profile could be responsible of the fatal hepatic damage observed in infected B6.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>18565585</pmid><doi>10.1016/j.molimm.2008.05.004</doi><tpages>9</tpages></addata></record> |
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| ispartof | Molecular immunology, 2008-08, Vol.45 (13), p.3580-3588 |
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| subjects | Animals Chagas Disease - genetics Chagas Disease - mortality Chagas Disease - parasitology Chagas Disease - pathology Female Gene Expression Regulation Heart - parasitology Hepatic injury Inflammation Inflammation Mediators - metabolism Liver - metabolism Liver - parasitology Liver - pathology Mice Mice, Inbred BALB C - genetics Mice, Inbred BALB C - metabolism Mice, Inbred BALB C - parasitology Mice, Inbred C57BL - genetics Mice, Inbred C57BL - metabolism Mice, Inbred C57BL - parasitology Myocardium - metabolism Myocardium - pathology Parasite infection Signal Transduction - genetics Spleen - metabolism Spleen - pathology Survival Analysis Toll-like receptor Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism Toll-Like Receptor 9 - genetics Toll-Like Receptor 9 - metabolism Trypanosoma cruzi Trypanosoma cruzi - immunology |
| title | TLR2, TLR4 and TLR9 are differentially modulated in liver lethally injured from BALB/c and C57BL/6 mice during Trypanosoma cruzi acute infection |
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