Maternal triacylglycerol signature and risk of food allergy in offspring.
Food allergy
lipidomics
timing of first solid-food introduction
triacylglycerol
Journal
The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
received:
09
09
2018
revised:
20
02
2019
accepted:
15
03
2019
pubmed:
21
4
2019
medline:
30
5
2020
entrez:
21
4
2019
Statut:
ppublish
Résumé
The prevalence of IgE-mediated food allergy (FA) is increasing worldwide, but the underlying mechanisms are poorly understood. We sought to examine the role of maternal lipidomic profiles in risk of FA development in offspring and to investigate the potential modification effects by timing of first solid-food introduction. This report included 1068 mother-child dyads from the Boston Birth Cohort. Maternal lipid metabolites in plasma were assessed by using liquid chromatography tandem mass spectrometry. Food sensitization (FS) was defined as a specific IgE level of 0.35 kU/L or greater to any of the 8 common food allergens determined by using ImmunoCAP. FA was defined based on FS, clinical symptoms, and food avoidance. Logistic regression was applied to analyze associations between maternal metabolites and risk of FS and FA in offspring and to explore potential effect modifications. Of the 1068 children, 411 had FS, and 132 had FA. Among the 209 metabolites, maternal triacylglycerols (TAGs) of shorter carbon chains and fewer double bonds were associated with greater risk of FA, whereas TAGs of longer carbon chains and more double bonds were significantly associated with lower risk of FA in offspring. These associations were stronger in children with delayed solid-food introduction (≥7 months of age) than those with earlier solid-food introduction (P = .010 for interaction between the maternal TAG score and timing of solid-food introduction). No significant association was found for FS. This is the first study to demonstrate a link between maternal TAGs and risk of FA in offspring and potential risk modification by timing of solid-food introduction.
Sections du résumé
BACKGROUND
The prevalence of IgE-mediated food allergy (FA) is increasing worldwide, but the underlying mechanisms are poorly understood.
OBJECTIVE
We sought to examine the role of maternal lipidomic profiles in risk of FA development in offspring and to investigate the potential modification effects by timing of first solid-food introduction.
METHODS
This report included 1068 mother-child dyads from the Boston Birth Cohort. Maternal lipid metabolites in plasma were assessed by using liquid chromatography tandem mass spectrometry. Food sensitization (FS) was defined as a specific IgE level of 0.35 kU/L or greater to any of the 8 common food allergens determined by using ImmunoCAP. FA was defined based on FS, clinical symptoms, and food avoidance. Logistic regression was applied to analyze associations between maternal metabolites and risk of FS and FA in offspring and to explore potential effect modifications.
RESULTS
Of the 1068 children, 411 had FS, and 132 had FA. Among the 209 metabolites, maternal triacylglycerols (TAGs) of shorter carbon chains and fewer double bonds were associated with greater risk of FA, whereas TAGs of longer carbon chains and more double bonds were significantly associated with lower risk of FA in offspring. These associations were stronger in children with delayed solid-food introduction (≥7 months of age) than those with earlier solid-food introduction (P = .010 for interaction between the maternal TAG score and timing of solid-food introduction). No significant association was found for FS.
CONCLUSION
This is the first study to demonstrate a link between maternal TAGs and risk of FA in offspring and potential risk modification by timing of solid-food introduction.
Identifiants
pubmed: 31004614
pii: S0091-6749(19)30522-6
doi: 10.1016/j.jaci.2019.03.033
pmc: PMC6941352
mid: NIHMS1060168
pii:
doi:
Substances chimiques
Allergens
0
Triglycerides
0
Immunoglobulin E
37341-29-0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
729-737Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK040561
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI090727
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD041702
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI079872
Pays : United States
Organisme : NICHD NIH HHS
ID : R21 HD085556
Pays : United States
Organisme : NICHD NIH HHS
ID : R03 HD096136
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES011666
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD086013
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 American Academy of Allergy, Asthma & Immunology. All rights reserved.
Références
Pediatrics. 2009 Dec;124(6):1549-55
pubmed: 19917585
J Allergy Clin Immunol. 2010 Oct;126(4):798-806.e13
pubmed: 20920770
Sci Transl Med. 2010 May 26;2(33):33ra37
pubmed: 20505214
J Neurosci. 2009 Jan 14;29(2):359-70
pubmed: 19144836
J Allergy Clin Immunol. 2018 Jun;141(6):2094-2106
pubmed: 29731129
J Allergy Clin Immunol. 2014 Feb;133(2):291-307; quiz 308
pubmed: 24388012
J Allergy Clin Immunol. 2015 Jan;135(1):171-8
pubmed: 25129677
J Allergy Clin Immunol. 2011 Jul;128(1):110-115.e5
pubmed: 21489610
J Allergy Clin Immunol. 2016 Jan;137(1):68-74.e4
pubmed: 26148797
Nat Med. 2011 Apr;17(4):448-53
pubmed: 21423183
J Allergy Clin Immunol. 2018 May;141(5):1668-1676.e16
pubmed: 29421277
Curr Allergy Asthma Rep. 2009 May;9(3):179-85
pubmed: 19348717
JAMA. 2016 Sep 20;316(11):1181-1192
pubmed: 27654604
J Allergy Clin Immunol Pract. 2016 Jul-Aug;4(4):713-20
pubmed: 27133095
Pediatrics. 2010 Jan;125(1):50-9
pubmed: 19969611
Lipids. 2007 Sep;42(9):801-10
pubmed: 17952480
Proc Nutr Soc. 2010 Aug;69(3):373-80
pubmed: 20462467
J Allergy Clin Immunol. 2009 Apr;123(4):940-8.e10
pubmed: 19135238
J Allergy Clin Immunol. 2008 Jun;121(6):1331-6
pubmed: 18539191
Am J Physiol Endocrinol Metab. 2013 Oct 1;305(7):E853-67
pubmed: 23921144
J Allergy Clin Immunol. 2010 Jun;125(6):1322-6
pubmed: 20462634
J Allergy Clin Immunol. 2010 Dec;126(6 Suppl):S1-58
pubmed: 21134576
J Lipid Res. 2013 Oct;54(10):2898-908
pubmed: 23868910
J Allergy Clin Immunol. 2013 Feb;131(2):442-50
pubmed: 23182172
Clin Chem. 2013 Nov;59(11):1657-67
pubmed: 23897902
J Allergy Clin Immunol. 2009 Nov;124(5):1031-8.e1-4
pubmed: 19733904
J Allergy Clin Immunol. 2008 Feb;121(2):464-470.e6
pubmed: 17980419
Stat Methods Med Res. 2017 Dec;26(6):2505-2525
pubmed: 26329750
N Engl J Med. 2015 Feb 26;372(9):803-13
pubmed: 25705822
Clin Exp Allergy. 2003 Oct;33(10):1360-7
pubmed: 14519141
Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1571-5
pubmed: 20080599
Clin Transl Allergy. 2015 Apr 02;5:16
pubmed: 25861446
J Allergy Clin Immunol. 2004 Dec;114(6):1398-402
pubmed: 15577844
Clin Exp Allergy. 2008 Jan;38(1):178-84
pubmed: 18028461
Curr Protoc Mol Biol. 2012 Apr;Chapter 30:Unit 30.2.1-24
pubmed: 22470063
J Allergy Clin Immunol. 2011 Aug;128(2):374-81.e2
pubmed: 21689850
J Clin Endocrinol Metab. 2016 Mar;101(3):871-9
pubmed: 26709969
J Allergy Clin Immunol. 2016 Jan;137(1):108-117
pubmed: 26194543
Lancet. 2013 Nov 16;382(9905):1656-64
pubmed: 23845860
J Clin Invest. 2011 Apr;121(4):1402-11
pubmed: 21403394
JAMA. 2014 Feb 12;311(6):587-96
pubmed: 24519298