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- W1966279337 abstract "Introduction: Biliary atresia is an inflammatory obstructive cholangiopathy of unknown etiology, in which genetic, infectious and environmental (toxic) factors have been proposed. The CD14 and tumor necrosis factor-alpha (TNF-alpha) promoter polymorphisms affect host susceptibility and immune responses to infectious agents like bacterial endotoxin and viral stimuli. Methods: We obtained genomic DNA from 90 patients with established diagnosis of biliary atresia and 143 healthy control children with the same ethnic group. The genotypes of CD14/C (-159, or termed as -260)T and TNF-alpha/G(-308)A (G allele, TNF*1; A allele, TNF*2) were determined by respective polymer-ase chain reaction and creation of HaeIII or NcoI restriction fragment assay. Plasma soluble CD14 levels (sCD14) were determined in different disease stages and genotypes of biliary atresia. Results: The frequencies of T allele and T/T homozygosity of the CD14/-159 promoter polymorphism were significantly higher in patients with biliary atresia (T allele 61.7 %, T/T genotype 42.2 %) than in control subjects (T allele 52.1%, T/T genotype 24.5%; P= 0.043 and 0.004, respectively). Decrease of plasma sCD14 from the early stage of biliary atresia when the patients received a Kasai operation to the late stage of liver cirrhosis was observed in carriers of the T/T and T/C genotypes, but not in carriers of the C/C genotype. The TNF-alpha/-308 promoter polymorphisms (TNF*1 and TNF*2) were studied and found not associated with biliary atresia. Conclusion: These findings show that genetic variants of the CD14 gene might influence the inflammatory response of the infants’ hepatobiliary system to exposure of infectious agents and are associated with the development and progression of biliary atresia." @default.
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- W1966279337 date "2004-06-01" @default.
- W1966279337 modified "2023-09-26" @default.
- W1966279337 title "P0192 PROMOTER POLYMORPHISM OF THE CD14 ENDOTOXIN RECEPTOR GENE IS ASSOCIATED WITH BILIARY ATRESIA" @default.
- W1966279337 doi "https://doi.org/10.1097/00005176-200406001-00316" @default.
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