Trypanosoma cruzi Infection in Genetically Selected Mouse Lines: Genetic Linkage with Quantitative Trait Locus Controlling Antibody Response. (12th August 2014)

• Record Type: Journal Article
• Authors: Vorraro, Francisca; Cabrera, Wafa H. K.; Ribeiro, Orlando G.; Jensen, José Ricardo; De Franco, Marcelo; Ibañez, Olga M.; Starobinas, Nancy
• Other Names: Chevillard Christophe Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2014(2014)
• Publication Date: 2014-08-12
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2014/952857
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Trypanosoma cruzi infection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high (H I I I ) or low (L I I I ) antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain—the high responder lines AIRmax and H I I I were resistant. The higher resistance of H I I I as compared to L I I I 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 H I I I 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(H I I I × L I I I ) × L I I I ] 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.