Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response
Trypanosoma cruzi infection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high (HIII) or low (LIII) antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain—the high responder lines AIRm...
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Wiley
2014-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2014/952857 |
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author | Francisca Vorraro Wafa H. K. Cabrera Orlando G. Ribeiro José Ricardo Jensen Marcelo De Franco Olga M. Ibañez Nancy Starobinas |
author_facet | Francisca Vorraro Wafa H. K. Cabrera Orlando G. Ribeiro José Ricardo Jensen Marcelo De Franco Olga M. Ibañez Nancy Starobinas |
author_sort | Francisca Vorraro |
collection | DOAJ |
description | Trypanosoma cruzi infection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high (HIII) or low (LIII) antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain—the high responder lines AIRmax and HIII were resistant. The higher resistance of HIII as compared to LIII mice extended to higher infective doses and was correlated with enhanced production of IFN-γ and nitric oxide production by peritoneal and lymph node cells, in HIII males and females. We also analyzed the involvement of previously mapped Ab and T. cruzi response QTL with the survival of Selection III mice to T. cruzi infections in a segregating backcross [F1(HIII×LIII) ×LIII] population. An Ab production QTL marker mapping to mouse chromosome 1 (34.8 cM) significantly cosegregated with survival after acute T. cruzi infections, indicating that this region also harbors genes whose alleles modulate resistance to acute T. cruzi infection. |
format | Article |
id | doaj-art-2bba11a411fb41209101ba79d3731a5c |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2014-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-2bba11a411fb41209101ba79d3731a5c2025-02-03T01:23:08ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/952857952857Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody ResponseFrancisca Vorraro0Wafa H. K. Cabrera1Orlando G. Ribeiro2José Ricardo Jensen3Marcelo De Franco4Olga M. Ibañez5Nancy Starobinas6Laboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilLaboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilLaboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilLaboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilLaboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilLaboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilLaboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, BrazilTrypanosoma cruzi infection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high (HIII) or low (LIII) antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain—the high responder lines AIRmax and HIII were resistant. The higher resistance of HIII as compared to LIII mice extended to higher infective doses and was correlated with enhanced production of IFN-γ and nitric oxide production by peritoneal and lymph node cells, in HIII males and females. We also analyzed the involvement of previously mapped Ab and T. cruzi response QTL with the survival of Selection III mice to T. cruzi infections in a segregating backcross [F1(HIII×LIII) ×LIII] population. An Ab production QTL marker mapping to mouse chromosome 1 (34.8 cM) significantly cosegregated with survival after acute T. cruzi infections, indicating that this region also harbors genes whose alleles modulate resistance to acute T. cruzi infection.http://dx.doi.org/10.1155/2014/952857 |
spellingShingle | Francisca Vorraro Wafa H. K. Cabrera Orlando G. Ribeiro José Ricardo Jensen Marcelo De Franco Olga M. Ibañez Nancy Starobinas Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response Mediators of Inflammation |
title | Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response |
title_full | Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response |
title_fullStr | Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response |
title_full_unstemmed | Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response |
title_short | Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response |
title_sort | trypanosoma cruzi infection in genetically selected mouse lines genetic linkage with quantitative trait locus controlling antibody response |
url | http://dx.doi.org/10.1155/2014/952857 |
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