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
Hauptverfasser: Carrera-Silva, Eugenio Antonio, Carolina, Cano Roxana, Natalia, Guiñazu, Pilar, Aoki Maria, Andrea, Pellegrini, Gea, Susana
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container_end_page 3588
container_issue 13
container_start_page 3580
container_title Molecular immunology
container_volume 45
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
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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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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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