Effects of endotoxin exposure on childhood asthma risk are modified by a genetic polymorphism in ACAA1Report as inadecuate




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BMC Medical Genetics

, 12:158

Genetic epidemiology and genetic associations

Abstract

BackgroundPolymorphisms in the endotoxin-mediated TLR4 pathway genes have been associated with asthma and atopy. We aimed to examine how genetic polymorphisms in innate immunity pathways interact with endotoxin to influence asthma risk in children.

MethodsIn a previous analysis of 372 children from the Boston Home Allergens and the Connecticut Childhood Asthma studies, 7 SNPs in 6 genes CARD15, TGFB1, LY96, ACAA1, DEFB1 and IFNG involved in innate immune pathways were associated with asthma, and 5 SNPs in 3 genes CD80, STAT4, IRAK2 were associated with eczema. We tested these SNPs for interaction with early life endotoxin exposure n = 291, in models for asthma and eczema by age 6.

ResultsWe found a significant interaction between endotoxin and a SNP rs156265 in ACAA1 p = 0.0013 for interaction. Increased endotoxin exposure by quartile showed protective effects for asthma in individuals with at least one copy of the minor allele OR = 0.39 per quartile increase in endotoxin, 95% CI 0.15 to 1.01. Endotoxin exposure did not reduce the risk of asthma in children homozygous for the major allele.

ConclusionOur findings suggest that protective effects of endotoxin exposure on asthma may vary depending upon the presence or absence of a polymorphism in ACAA1.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2350-12-158 contains supplementary material, which is available to authorized users.

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Author: Joanne E Sordillo - Sunita Sharma - Audrey Poon - Jessica Lasky-Su - Kathleen Belanger - Donald K Milton - Michael B Bra

Source: https://link.springer.com/







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