Department of Population, Family and Reproductive Health, Center on the Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md.
Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Mass; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston Mass.
J Allergy Clin Immunol. 2019 Sep;144(3):729-737. doi: 10.1016/j.jaci.2019.03.033. Epub 2019 Apr 18.
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.
IgE 介导的食物过敏（FA）的患病率在全球范围内呈上升趋势，但发病机制尚不清楚。
本研究旨在探讨母体脂质组学特征在后代 FA 发病风险中的作用，并研究首次引入固体食物时间的潜在修饰作用。
本报告纳入了来自波士顿出生队列的 1068 对母婴对子。采用液相色谱串联质谱法检测血浆中的母体脂质代谢物。食物致敏（FS）定义为 0.35 kU/L 或更高的任何 8 种常见食物过敏原的特异性 IgE 水平，通过 ImmunoCAP 测定。FA 根据 FS、临床症状和食物回避来定义。应用逻辑回归分析母体代谢物与后代 FS 和 FA 发病风险之间的关联，并探讨潜在的效应修饰作用。
在 1068 名儿童中，411 名儿童有 FS，132 名儿童有 FA。在 209 种代谢物中，母体三酰甘油(TAG)的碳链较短且双键较少与 FA 的发病风险增加相关，而碳链较长且双键较多的 TAG 与后代 FA 的发病风险降低显著相关。在首次引入固体食物（≥7 个月）时间较晚的儿童中，这些关联更为明显（母体 TAG 评分与固体食物引入时间之间的交互作用 P = 0.010）。FS 与母体 TAG 无显著关联。
这是首个表明母体 TAG 与后代 FA 发病风险之间存在关联，并与固体食物引入时间有关的潜在风险修饰作用的研究。
