Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5918365 | Molecular Immunology | 2008 | 6 Pages |
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, â62A/T and â262A/G, in the promoter of IKBL by PCR-RFLP analysis in 169 patients with CCC and 76 ASY. Genotype distributions for both â62A/T and â262A/G differed between the CCC and ASY (Ï2 = 7.3; P = 0.025 and Ï2 = 6.8; P = 0.03, respectively). Subjects, homozygous for the â62A 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 â262A homozygotes (P = 0.005; OR = 2.7 [95% CI 1.3-6.0]. The haplotype â262A â62A 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.
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Authors
Rajendranath Ramasawmy, Kellen C. Faé, Edecio Cunha-Neto, Susan C.P. Borba, Barbara Ianni, Charles Mady, Anna C. Goldberg, Jorge Kalil,