TITLE

Linkage of Crohn's disease-related serological phenotypes: NFKB1 haplotypes are associated with anti-CBir1 and ASCA, and show reduced NF-κB activation

AUTHOR(S)
Takedatsu, H.; Taylor, K. D.; Mei, L.; McGovern, D. P. B.; Landers, C. J.; Gonsky, A.; Cong, Y.; Vasiliauskas, E. A.; Ippoliti, A.; Elson, C. O.; Rotter, J. I.; Targan, S. A.
PUB. DATE
January 2009
SOURCE
Gut;Jan2009, Vol. 58 Issue 1, p60
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background and aims: Genetics studies of the serum expression of antibodies to microbial antigens may yield important clues to the pathogenesis of Crohn's disease. Our aim was to conduct a linkage study using expression of anti-CBiri, anti-12, anti-OmpC and ASCA as quantitative traits. Methods: Expression of antibodies to microbial antigens was measured by enzyme-linked immunosorbant assay (ELISA) and a standard -10 cM whole genome microsatellite study was conducted. Single nucleotide polymorphism genotyping was performed using either Illumina or TaqMan MGB technology. Nuclear factor Kappa B (NE-κB) activation in cells from Epstein-Barr virus (EBV)-transformed cell lines was assessed using an electrophoretic mobility shift assay and protein was measured using ELISA and western blotting. Results: Evidence for linkage to anti-CBirl expression was detected on human chromosome 4 (logarithm of odds (LOD) 1.82 at 91 cM(. We therefore directly proceeded to test the association of haplotypes in NFKB1, a candidate gene. One haplotype, Hi, was associated with anti-CBirl (p = 0.003) and another, H3, was associated with ASCA (p = 0.023). Using cell lines from Crohn's disease patients with either Hi or H3, NE-κB activation and NE-κB p105 and p50 production were significantly lower for patients with Hi compared to patients with H3. Conclusions: These results suggest that NFKB1 haplo- types induce dysregulation of innate immune responses by altering NF-κB expression. The results also show the use of EBV-transformed lymphoblastoid cell lines to conduct phenotypic studies of genetic variation.
ACCESSION #
35965708

 

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