Article ID Journal Published Year Pages File Type
5918365 Molecular Immunology 2008 6 Pages PDF
Abstract
Chagas' disease, caused by Trypanosoma cruzi, is an inflammatory disorder leading to chronic Chagas cardiomyopathy (CCC). Only one third of T. cruzi-infected individuals progress to CCC while the others are considered asymptomatic (ASY). The human inhibitory κB-like gene (IKBL/NFKBIL1), homologous to the IκB family of proteins that regulate the NFκB family of transcription factors, is suggested as a putative inhibitor of NFκB. We investigated two functional polymorphisms, −62A/T and −262A/G, in the promoter of IKBL by PCR-RFLP analysis in 169 patients with CCC and 76 ASY. Genotype distributions for both −62A/T and −262A/G differed between the CCC and ASY (χ2 = 7.3; P = 0.025 and χ2 = 6.8; P = 0.03, respectively). Subjects, homozygous for the −62A allele, had three-fold risk of developing CCC compared with those carrying the TT genotype (P = 0.0095; Odds Ratio [OR] = 2.9; [95% CI 1.2-7.3]). Similar trend was observed for the −262A homozygotes (P = 0.005; OR = 2.7 [95% CI 1.3-6.0]. The haplotype −262A −62A was prevalent in patients with CCC (40% versus 24%; OR 2.1 [95% CI 1.4-3.3]; Pc = 0.0014). The IKBL locus itself or another critical gene in this region may confer susceptibility to the development of CCC.
Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Molecular Biology
Authors
, , , , , , , ,