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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Main Authors: Francisca Vorraro, Wafa H. K. Cabrera, Orlando G. Ribeiro, José Ricardo Jensen, Marcelo De Franco, Olga M. Ibañez, Nancy Starobinas
Format: Article
Language:English
Published: Wiley 2014-01-01
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.
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institution Kabale University
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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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