Journal of Clinical Toxicology
Open Access
ISSN: 2161-0495
+44 1478 350008
ISSN: 2161-0495
+44 1478 350008
Humberto Mendoza
Scientific Tracks Abstracts: J Clinic Toxicol
C hagas disease caused by T. cruzi 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 T. cruzi 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-�?±, IL1-�?², 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