Exploring Novel Management to Reduce Preterm Birth: The Role of In Molecular Hydrogen Production and Th17

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K16812
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 56040:Obstetrics and gynecology-related
• Research Institution: Nagoya University
• Principal Investigator: IMAI Kenji 名古屋大学, 医学部附属病院, 講師 (20778295)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 早産 / 分子状水素 / T細胞 / 胎児脳障害 / IL-26

Outline of Final Research Achievements

We investigated the association between molecular hydrogen (H2) concentration and preterm birth, as well as the effectiveness of maternal H2 administration from an immunological perspective. Using both mouse models and samples from pregnant women (breath, serum, T cells, amniotic membrane etc.), we demonstrated that in vivo H2 concentration is an independent causal factor for preterm birth. H2 was found to inhibit effector T cells such as CD8, Th1, and Th17, without affecting Tregs, thereby supporting the maintenance of immune tolerance necessary for pregnancy. The study also identified a subgroup of pregnant women with low in vivo H2 levels who are at high risk for preterm birth and suggested that H2 supplementation could be a potential preventive and therapeutic approach for preterm birth.

Free Research Field

産婦人科

Academic Significance and Societal Importance of the Research Achievements

生体内H2濃度の低い妊婦は早産ハイリスクであった。生体内H2濃度低下と出生児脳障害の関連も既に報告した。母獣や胎仔のH2濃度の意義を世界に先駆けて報告してきたが、本研究はこれら知見をヒト妊婦で確認した初めての研究であろう。Ｈ2濃度は呼気検査により簡便・低侵襲に測定でき、早産予測マーカーとして臨床応用する実現性は高い。母体の免疫細胞Th17、新規炎症性サイトカインIL-26が早産に関わること、生体内Ｈ2がeffector T細胞の活性化を抑制することを初めて報告した。これら成果は腸管内Ｈ2濃度の低い集団を対象としたH2の補完・補充が早産減少や後遺症なき児生存の一助となる可能性を期待させる。