Key result
Infected susceptible Balb/c mice demonstrated significantly lower cardiac output compared to resistant C57BL/6J mice (13.1 vs 18.7 mL/min, P=0.002), associated with differential expression of the AKT gene network.
Why the study?
Does acute Trypanosoma cruzi infection induce differential myocardial contractility and gene expression changes in susceptible versus resistant mice strains?
Does acute Trypanosoma cruzi infection induce differential myocardial contractility and gene expression changes in susceptible versus resistant mice strains?
Acute Chagasic myocarditis induces strain-specific reductions in cardiac output and contractility that are associated with differential regulation of the host AKT gene network.
Supports host genetic studies in Chagas myocarditis; leaves open AKT network as therapeutic target in humans.
Chagasic disease is associated with high morbidity in Latin America. Acute Chagasic myocarditis is consistently found in acute infections, but little is known about its contribution to chronic cardiomyopathy. The aim of the study was to phenotypically characterize two strains of mice with differential Chagas infection susceptibility and correlate strain myocarditis phenotypes with heart tissue gene expression. C57BL/6J and Balb/c mice were injected intraperitoneally with 0 or 150-200 tissue-derived trypomastigotes (Tulahuen strain). Echocardiograms, brain natriuretic peptide, and troponin were measured. Heart tissue was harvested for histopathological analysis and gene expression profiling on microarrays. Genes differently expressed between infected Balb/c and C57BL/6J mice were identified. Echocardiograms showed differences in Balb/c versus C57BL/6J infected mice in heart rate (413 versus 476 beats per minute; P = 0.0001), stroke volume (31.9 ± 9.3 versus 39.2 ± 5.5 μL; P = 0.03), and cardiac output (13.1 ± 3.5 versus 18.7 ± 3.2 μL/min; P = 0.002). Gene expression at 4 weeks analysis showed 32 statistically significant (q value < 0.05) differentially expressed genes between infected Balb/c and C57BL/6J mice that were enriched for genes related to the protein kinase B (AKT) pathway. These specific phenotypic features of cardiac response during acute Chagasic myocarditis may, in part, be related to host AKT network regulation.
No takes yet. Share an insight, caveat, or question.
Henao‐Martínez et al. (2015) studied Acute Chagasic myocarditis (n=48). Trypanosoma cruzi infection (Tulahuen strain) vs. Uninfected control mice and resistant C57BL/6J strain was evaluated on Cardiac output at 4 weeks post-infection (p=0.002). Infected susceptible Balb/c mice demonstrated significantly lower cardiac output compared to resistant C57BL/6J mice (13.1 vs 18.7 mL/min, P=0.002), associated with differential expression of the AKT gene network.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: