Friday, 15th December 2017
Cell Biology and Immunology
    Immunoregulatory mechanisms in the development of Chagas disease: translational applications

 


Grupo-400

 


 

 

Núria Gironès Pujol

 ASciStaff

APublications

 

 

 

 

Research summary:

Chagas disease caused Trypanosoma cruzi affects approximately 10 million people in Latin America. Besides, blood transfusion and organ transplantation is a sanitary problem in countries receptors of migrants from endemic areas. Cardiac pathology is the most severe and characteristic manifestation and it is estimated a future incidence between 6.000 y 30.000 cases of chagasic cardiomyopathy in Spain.

Our working hypothesis is that development of pathology depends on a combination of factors: host genetic background, different parasite infecting capacities with different genetic backgrounds and the regulatory immune response will affect the inflammatory process. In this context, our goal is the study of the regulatory response, through myeloid-derived suppressor cells and regulatory T cells during experimental infection in the mouse model, further studying and identifying regulatory cell populations in the inflammatory infiltrate implicated in controlling parasite replication and/or tissue damage.

On the other hand, during infection, cardiac damage is not directly related to parasite burden in heart tissue, thus, it is postulated that autoimmune mechanisms might be contributing to Chagas pathology. In this regard, our objective is to determine the role of the possible autoimmune mechanisms in the development of cardiomyopathy.

Our interest for translational application of our research let us to maintain scientific collaborations with Spanish and foreign groups, basic and clinical, for the evaluation of new prognostic and follow up biomarkers, needed for deciding treatment of patients and its efficacy.

 

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Relevant publications:

  • Global Metabolomic Profiling of Acute Myocarditis Caused by Trypanosoma cruzi Infection. Gironès N*, Carbajosa S, Guerrero NA, Poveda C, Chillón-Marinas C, Fresno M. PLoS Negl Trop Dis. 2014 Nov 20;8(11):e3337. (*Corresponding author.)
  • Analysis of the Dynamics of Infiltrating CD4(+) T Cell Subsets in the Heart during Experimental Trypanosoma cruzi Infection. Sanoja C, Carbajosa S, Fresno M*, Gironès N*. PLoS One. 2013 Jun 11;8(6):e65820. (*Both authors contributed equally to the direction of this work.)
  • Myeloid-derived suppressor cells infiltrate the heart in acute Trypanosoma cruzi infection. Cuervo H, Guerrero NA, Carbajosa S, Beschin A, De Baetselier P, Gironès N*, Fresno M*.. J Immunol. 2011 Sep 1;187(5):2656-65. (*Both authors contributed equally to the direction of this work.)
  • Nitric Oxide Synthase and Arginase Expression in Heart Tissue during Acute Trypanosoma cruzi Infection in Mice: Arginase I Is Expressed in Infiltrating CD68(+) Macrophages. Cuervo H., Pineda M. A., Aoki M. P., Gea S., Fresno M*. and Gironès N*. Inducible Nitric J Infect Dis. 2008 May 12. (*Both authors contributed equally to the direction of this work.)
  • Dominant T- and B-cell epitopes in an autoantigen linked to Chagas' disease. Gironès N*, Rodríguez CI*, Carrasco-Marín E, Hernáez RF, de Rego JL, Fresno M. J Clin Invest. 2001 Apr;107(8):985-93. (*Both authors contributed equally to this work.)