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Mediators of Inflammation
Volume 2014 (2014), Article ID 952857, 15 pages
Research Article

Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response

Laboratório de Imunogenética, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, Brazil

Received 24 April 2014; Revised 15 July 2014; Accepted 16 July 2014; Published 13 August 2014

Academic Editor: Christophe Chevillard

Copyright © 2014 Francisca Vorraro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Trypanosoma cruzi infection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high () or low () antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain—the high responder lines AIRmax and were resistant. The higher resistance of as compared to mice extended to higher infective doses and was correlated with enhanced production of IFN- and nitric oxide production by peritoneal and lymph node cells, in 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( ) ] 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.