特定の脂肪酸を血中に持たない母親は子どもの喘息リスクが高い（Mothers without specific fatty acid in the blood more often have children with asthma）

2026-05-01 コペンハーゲン大学（UCPH）

＜関連情報＞

• https://news.ku.dk/all_news/2026/05/mothers-without-specific-fatty-acid-in-the-blood-more-often-have-children-with-asthma/
• https://www.sciencedirect.com/science/article/pii/S2666379126001060

母親の12-HETE濃度は、小児喘息および出生前オメガ3サプリメント摂取への反応と関連している Maternal 12-HETE is associated with childhood asthma and the responses to prenatal omega-3 supplementation

Liang Chen ∙ Nicklas Brustad ∙ Jonathan Thorsen ∙ … ∙ Klaus Bønnelykke ∙ Jakob Stokholm ∙ Bo Chawes
Cell Reports Medicine  Published: March 17, 2026
DOI:https://doi.org/10.1016/j.xcrm.2026.102689

Graphical abstract

Highlights

• Maternal 12-HETE levels associate with childhood asthma risk
• Maternal 12-HETE levels relate to infant airway microbiota and immune patterns
• Higher prenatal n-3 LCPUFA intake reduced childhood asthma risk in offspring
• Effect of prenatal n-3 LCPUFA intake varies by maternal 12-HETE status

Summary

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.