Linked Life Data

19460328

Source:http://linkedlifedata.com/resource/pubmed/id/19460328

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pubmed-article:19460328pubmed:abstractTextLeprosy is an infectious disease caused by Mycobacterium leprae. The peptide human beta-defensin 1 is an antimicrobial effector of innate epithelial immunity. A study was done on the association of three single nucleotide polymorphisms (SNPs) in the beta-defensin 1 gene (DEFB1) - 668 C/G (-44 C/G or rs1800972; in 5' UTR), 692 A/G (-20 A/G or rs11362; in 5' UTR) and A1836G (rs1800971; in 3' UTR) - with leprosy susceptibility per se and clinical leprosy variants. The SNPs were genotyped by real-time polymerase chain reaction (rt-PCR) and PCR-restriction fragment length polymorphisms. Subjects were of Mexican mestizo ethnicity from Sinaloa state, México. Analysis was done on borderline leprosy, lepromatous leprosy (L-lep) and indeterminate leprosy subgroups compared with healthy controls. Results: The genotypes associated with L-lep and no other leprosy subgroup after Bonferroni correction were those that contain 668C in a dominant model (OR=3.06, 95% CI 1.47-6.4, p=0.024). Estimated haplotype CGA is over-represented in L-lep (p=0.009; OR=2.25, 1.23-4.03). Five NF-kappaB1 putative binding sites (NPBSs) were identified with JASPAR software in non-coding strand spanning the 5' UTR and intron 1 of DEFB1, including one which is altered when SNP 668C is present. SNP 668C probably abrogates NF-kappaB-dependent DEFB1 upregulation leading to L-lep variant.lld:pubmed
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pubmed-article:19460328pubmed:pagination617-25lld:pubmed
pubmed-article:19460328pubmed:dateRevised2009-11-27lld:pubmed
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pubmed-article:19460328pubmed:articleTitleSNP 668C (-44) alters a NF-kappaB1 putative binding site in non-coding strand of human beta-defensin 1 (DEFB1) and is associated with lepromatous leprosy.lld:pubmed
pubmed-article:19460328pubmed:affiliationGuadalajara University, Guadalajara, Jalisco, Mexico. eprado@ciatej.net.mxlld:pubmed
pubmed-article:19460328pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19460328pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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