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hagas disease caused by
is endemic in Latin America and an emerging disease in the US and other developed
countries. The clinical course of the disease can be broadly categorized into three stages� Initial, Intermediate, and Chronic.
Chagas disease pathogenesis has previously been shown to be associated with inflammatory responses including ROS production.
In this study, we examined key events related to innate immune responses in Chagasic patients. Previously, RNA isolated from
infected macrophages was used to profile the expression of 84 key genes involved in innate immunity as well as in toll-like
and NOD-like receptor signaling by RT-PCR arrays (QIAGEN Inc., CA).Twelve genes expressing inflammasome components
(AIM2, NLRP3, NLRC5), toll-like receptors (TLR2,TLR9), adaptor molecules (MYD88), cytokines or chemokines (TNF-α, IL1-β,
CCL2, CXCL1, CXCL2), and cellular transcription factors (NFkB-1A) were selected based on the results of the RT-PCR arrays
for further analysis in Chagasic patients. Real Time PCR was performed to quantify differential expression of these selected genes
in peripheral blood mononuclear cells (PBMCs) isolated from patients in various stages of Chaga�s disease along with PBMCs
isolated from normal healthy individuals. We saw an upregulation of gene expression of various receptors, transcription factors
and inflammasome components during the later stages of Chagas disease. However, due to the small pool of patients used in this
project, it is difficult to generate a definite statement regarding differential gene expression in specific stages of Chagas disease
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