Immunoregulatory mechanisms in the development of Chagas disease: translational applications

Research summary:

Chagas disease caused byTrypanosoma 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. 

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. For this, we use “Omics” tools as Genomics, Transcriptomics, Proteomics and Metabolomics.


* For external calls please dial 34 91196 followed by the extension number
Last nameNameLaboratoryExt.*e-mailProfessional category
Galán MartínezJavier2264593jgalan(at)cbm.csic.esTco. de Investigación y Laboratorio
Gironés PujolNuria126/114.34593/4735ngirones(at)cbm.csic.esProfesor Titular Universidad, GA
Moral SalmoralJavier del126/2264735Tco. de Investigación y Laboratorio

Relevant publications:

  • Genomic assemblies of newly sequenced Trypanosoma cruzi strains reveal new genomic expansion and greater complexity. Callejas-Hernández F, C., Rastrojo A, Poveda C, Gironès N1c and Fresno M1c. Scientific Reports, 2018. 8:14631. doi:10.1038/s41598-018-32877-2. IF: 4,259; Q1.
  • L-arginine supplementation reduces mortality and improves disease outcome in mice infected with Trypanosoma cruzi. Carbajosa S, Rodríguez-Angulo HO, Gea S, Chillón-Marinas C, Poveda C, Maza MC, Colombet D, Fresno M1Gironès N1c. PLoS Negl Trop Dis. 2018 Jan 16;12(1):e0006179. doi: 10.1371/journal.pntd.0006179. IF: 3,834; Q1.
  • Altered bone marrow lymphopoiesis and interleukin-6-dependent inhibition of thymocyte differentiation contribute to thymic atrophy during Trypanosoma cruzi infection. Carbajosa S, Gea S, Chillón-Marinas C, Poveda C, Del Carmen Maza M, Fresno M1Gironès N1c. Oncotarget. 2017 Mar 14;8(11):17551-17561. doi: 10.18632/oncotarget.14886. IF: 5,168; Q1.
  • Cyclooxygenase-2 and Prostaglandin E2 Signaling through Prostaglandin Receptor EP-2 Favor the Development of Myocarditis during Acute Trypanosoma cruzi Infection. Guerrero NA, Camacho M, Vila L, Íñiguez MA, Chillón-Marinas C, Cuervo H, Poveda C, Fresno M1Gironès N1c. PLoS Negl Trop Dis. 2015 Aug 25;9(8):e0004025. doi: 10.1371/journal.pntd.0004025. IF: 3,834; Q1.
  • Global metabolomic profiling of acute myocarditis caused by Trypanosoma cruzi infection. Gironès Nc, Carbajosa S, Guerrero NA, Poveda C, Chillón-Marinas C, Fresno M. PLoS Negl Trop Dis. 2014 Nov 20;8(11):e3337. doi: 10.1371/journal.pntd.0003337 IF: 3,834; Q1.
  • Analysis of the Dynamics of Infiltrating CD4(+) T Cell Subsets in the Heart during Experimental Trypanosoma cruzi Infection. Sanoja C, Carbajosa S, Fresno M1, Gironès N1c. PLoS One. 2013 Jun 11;8(6):e65820 . IF: 2,766; Q1.
  • Myeloid-derived suppressor cells infiltrate the heart in acute Trypanosoma cruzi infection. Cuervo H, Guerrero NA, Carbajosa S, Beschin A, De Baetselier P, Gironès N1c, Fresno M1. J Immunol. 2011 Sep 1;187(5):2656-65. IF: 5,788; Q1.
  • 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 M1. and Gironès N1c. Inducible Nitric J Infect Dis. 2008 May 12. IF: 5,682; Q1.

corresponding author. 1 equal contribution to the direction of the work

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