title: Distinct outcomes of Trypanosoma cruzi infection in hamsters are related to myocardial parasitism, cytokine/chemokine gene expression, and protein expression profile.
abstract: BACKGROUND
  Trypanosoma cruzi-infected outbred hamsters reproduce the range of different outcomes of Chagas disease noted in humans. We tested whether myocarditis, its mediators, and myocardial protein expression are related to the severity of the acute phase of T. cruzi infection in the hamster model.
  
  
  METHODS
  Myocardium left ventricles (LVs) obtained from Syrian hamsters infected with T. cruzi were collected 21 days after infection. Myocarditis and the T. cruzi nest/antigen area were analyzed by histological and morphometric analysis. Cytokine and chemokine messenger RNA (mRNA) expression was analyzed using real-time reverse-transcriptase polymerase chain reaction. Differentially expressed proteins were identified by 2-dimensional electrophoresis, followed by mass spectrometry.
  
  
  RESULTS
  While in the acute phase of infection, 50% of animals displayed weight loss and signs of acute-phase infection (hereafter referred to as "acute-phase signs" [APS]) (e.g., lethargy, vomiting, and diarrhea). Both the T. cruzi nest/antigen area and the expression of interferon-gamma, tumor necrosis factor-alpha, interleukin-10, and CCL3 mRNA were significantly increased in the LVs of animals with APS, compared with the LVs of animals without APS. Animals with APS, those without APS, and uninfected animals demonstrated distinct myocardial expression of contractile, stress response, and metabolism proteins.
  
  
  CONCLUSIONS
  The distinct outcomes of acute T. cruzi infection in Syrian hamsters are related to cardiac parasitism, cytokine expression, and changes in the expression of structural/contractile and stress response proteins that may be associated with alterations in the cardiomyocyte cytoskeleton.
authors.affiliation: Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.
authors.forename: Angelina M
authors.initials: AM
authors.lastname: Bilate
authors.forename: Priscila C
authors.initials: PC
authors.lastname: Teixeira
authors.forename: Susan P
authors.initials: SP
authors.lastname: Ribeiro
authors.forename: Thales de
authors.initials: Td
authors.lastname: Brito
authors.forename: Ana Maria
authors.initials: AM
authors.lastname: Silva
authors.forename: Momtchilo
authors.initials: M
authors.lastname: Russo
authors.forename: Jorge
authors.initials: J
authors.lastname: Kalil
authors.forename: Edecio
authors.initials: E
authors.lastname: Cunha-Neto
mesh_terms: D000818:Animals; D009202:Cardiomyopathies / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D002598:Chagas Cardiomyopathy / Q000097:blood / Q000503:physiopathology; D014355:Chagas Disease / Q000378:metabolism* / Q000503:physiopathology; D018925:Chemokines / Q000235:genetics / Q000378:metabolism*; D006224:Cricetinae; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D015870:Gene Expression; D051379:Mice; D009205:Myocarditis / Q000097:blood / Q000469:parasitology / Q000503:physiopathology; D014349:Trypanosoma cruzi / Q000276:immunology* / Q000378:metabolism
chemical_list: D018925:Chemokines; D016207:Cytokines