Dataset: Expression data from hearts of wild-type C57BL/6 mice infected with T. cruzi and controls (uninfected)

An efficient innate immune recognition of the intracellular parasite T. cruzi is crucial for host protection against development of Chagas disease, which often leads to multiple organ damage, particularly the heart leading to cardiomyopathy. Mechanisms modulated by MyD88 have been shown to be necessary for resistance against T, cruzi infection. Recently, Nod-like receptors have been shown to play an important role as innate immune sensors, particularly as they relate to inflammasome function, caspase activation, and inflammatory cytokine production. In this study, we aimed to investigate the participation of innate immune responses in general, and inflammasomes in particular, in heart inflammation and cardiac damage upon infection with the T. cruzi parasite. We used microarrays to gain insight into gene expression in the cardiac tissue of mice infected with the causative agent of Trypanosoma cruzi, and identified distinct classes of up-regulated genes during this process, including important genes involved in inflammasome activation and innate immune responses in general. The hearts of C57BL/6 mice day 18 post-infection with a Y strain of the parasite T. cruzi, and uninfected controls were extraced for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare gene expression among two groups of mice, and so extracted the hearts of 3 control uninfected mice, and of 3 infected mice 18 days post-infection.

Species:

mouse

Samples:

6

Source:

E-GEOD-41089

Updated:

Dec.12, 2014

Registered:

Nov.24, 2014