摘要
最近的一项小鼠研究表明，缺乏12-羟基二碳四烯酸（12-HETE）会影响新生儿肺泡巨噬细胞印迹，并与呼吸道疾病增加有关，但尚未在人类中进行研究。利用COPSAC2010和VDAART两个母婴队列的数据，我们证明，妊娠期间未检测到的母体血浆12-HETE与儿童哮喘和呼吸道感染的风险增加有关，同时婴儿气道微生物群结构和气道免疫谱也会发生改变。此外，在COPSAC2010的一项随机临床试验中，我们观察到母体12-HETE水平与母体N-3长链多不饱和脂肪酸（N-3 LCPUFA）补充之间的相互作用，以及VDAART中母体饮食N-3 LCPUFA摄入量与后代呼吸道疾病的关系；在可检测到12-HETE水平的母亲中，较高的产前n-3 LCPUFA暴露可减少哮喘和呼吸道感染。这些发现确定了母体12-HETE是后代呼吸系统疾病风险的潜在生物标志物，并表明母体12-HETE状态可能决定了产前n-3 LCPUFA补充的反应性。
Maternal 12-HETE is associated with childhood asthma and the responses to prenatal omega-3 supplementation
Liang Chen, Nicklas Brustad, Jonathan Thorsen, Tingting Wang, Mina Ali, Julie N Kyvsgaard, Mario Lovric, Parvaneh Ebrahimi, Yang Luo, Casper-Emil T Pedersen, Nicole Prince, Rachel S Kelly, Ann-Marie M Schoos, Nilo Vahman, Morten A Rasmussen, Susanne Brix, Augusto A Litonjua, Scott T Weiss, Craig E Wheelock, Jessica Lasky-Su, Klaus Bønnelykke, Jakob Stokholm, Bo Chawes
Abstract
A recent mouse study has shown that deficiency in 12-hydroxyeicosatetraenoic acid (12-HETE) affects neonatal alveolar macrophage imprinting and associates with increased respiratory morbidity, but this has not been investigated in humans. Utilizing data from two mother-child cohorts, COPSAC2010 and VDAART, we demonstrate that undetectable maternal plasma 12-HETE during pregnancy associates with increased risk of childhood asthma and respiratory infections alongside an altered infant airway microbiota structure and airway immune profile. Further, we observed an interaction between maternal 12-HETE levels and maternal N-3 long-chain polyunsaturated fatty acid (n-3 LCPUFA) supplementation in a randomized clinical trial in COPSAC2010 and maternal dietary n-3 LCPUFA intake in VDAART in relation to offspring respiratory morbidity; higher prenatal n-3 LCPUFA exposure reduced asthma and respiratory infection among mothers with detectable 12-HETE levels. These findings identify maternal 12-HETE as a potential biomarker for risk of offspring respiratory morbidity and suggest that maternal 12-HETE status may determine responsiveness to prenatal n-3 LCPUFA supplementation.
最近的一项小鼠研究表明，缺乏12-羟基二碳四烯酸（12-HETE）会影响新生儿肺泡巨噬细胞印迹，并与呼吸道疾病增加有关，但尚未在人类中进行研究。利用COPSAC2010和VDAART两个母婴队列的数据，我们证明，妊娠期间未检测到的母体血浆12-HETE与儿童哮喘和呼吸道感染的风险增加有关，同时婴儿气道微生物群结构和气道免疫谱也会发生改变。此外，在COPSAC2010的一项随机临床试验中，我们观察到母体12-HETE水平与母体N-3长链多不饱和脂肪酸（N-3 LCPUFA）补充之间的相互作用，以及VDAART中母体饮食N-3 LCPUFA摄入量与后代呼吸道疾病的关系；在可检测到12-HETE水平的母亲中，较高的产前n-3 LCPUFA暴露可减少哮喘和呼吸道感染。这些发现确定了母体12-HETE是后代呼吸系统疾病风险的潜在生物标志物，并表明母体12-HETE状态可能决定了产前n-3 LCPUFA补充的反应性。
（北京朝阳医院呼吸与危重症医学科 顾宪民 摘译 中日友好医院呼吸与危重症医学科 林江涛 审校）
（Cell Rep Med. 2026 Mar 17;7(3):102689. doi: 10.1016/j.xcrm.2026.102689.）
（Cell Rep Med. 2026 Mar 17;7(3):102689. doi: 10.1016/j.xcrm.2026.102689.）
Maternal 12-HETE is associated with childhood asthma and the responses to prenatal omega-3 supplementation
Liang Chen, Nicklas Brustad, Jonathan Thorsen, Tingting Wang, Mina Ali, Julie N Kyvsgaard, Mario Lovric, Parvaneh Ebrahimi, Yang Luo, Casper-Emil T Pedersen, Nicole Prince, Rachel S Kelly, Ann-Marie M Schoos, Nilo Vahman, Morten A Rasmussen, Susanne Brix, Augusto A Litonjua, Scott T Weiss, Craig E Wheelock, Jessica Lasky-Su, Klaus Bønnelykke, Jakob Stokholm, Bo Chawes
Abstract
A recent mouse study has shown that deficiency in 12-hydroxyeicosatetraenoic acid (12-HETE) affects neonatal alveolar macrophage imprinting and associates with increased respiratory morbidity, but this has not been investigated in humans. Utilizing data from two mother-child cohorts, COPSAC2010 and VDAART, we demonstrate that undetectable maternal plasma 12-HETE during pregnancy associates with increased risk of childhood asthma and respiratory infections alongside an altered infant airway microbiota structure and airway immune profile. Further, we observed an interaction between maternal 12-HETE levels and maternal N-3 long-chain polyunsaturated fatty acid (n-3 LCPUFA) supplementation in a randomized clinical trial in COPSAC2010 and maternal dietary n-3 LCPUFA intake in VDAART in relation to offspring respiratory morbidity; higher prenatal n-3 LCPUFA exposure reduced asthma and respiratory infection among mothers with detectable 12-HETE levels. These findings identify maternal 12-HETE as a potential biomarker for risk of offspring respiratory morbidity and suggest that maternal 12-HETE status may determine responsiveness to prenatal n-3 LCPUFA supplementation.
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