Gray Lawrence E K, O'Hely Martin, Ranganathan Sarath, Sly Peter David, Vuillermin Peter
Barwon Infant Study, School of Medicine, Deakin University, Geelong, VIC, Australia.
Child Health Research Unit, Barwon Health, Geelong, VIC, Australia.
Front Immunol. 2017 Mar 31;8:365. doi: 10.3389/fimmu.2017.00365. eCollection 2017.
This review focuses on the current evidence that maternal dietary and gut bacterial exposures during pregnancy influence the developing fetal immune system and subsequent offspring asthma. Part 1 addresses exposure to a farm environment, antibiotics, and prebiotic and probiotic supplementation that together indicate the importance of bacterial experience in immune programming and offspring asthma. Part 2 outlines proposed mechanisms to explain these associations including bacterial exposure of the fetoplacental unit; immunoglobulin-related transplacental transport of gut bacterial components; cytokine signaling producing fetomaternal immune alignment; and immune programming metabolites produced by gut bacteria. Part 3 focuses on the interplay between diet, gut bacteria, and bacterial metabolites. Maternal diet influences fecal bacterial composition, with dietary microbiota-accessible carbohydrates (MACs) selecting short-chain fatty acid (SCFA)-producing bacteria. Current evidence from mouse models indicates an association between increased maternal dietary MACs, SCFA exposure during pregnancy, and reduced offspring asthma that is, at least in part, mediated by the induction of regulatory T lymphocytes in the fetal lung. Part 4 discusses considerations for future studies investigating maternal diet-by-microbiome determinants of offspring asthma including the challenge of measuring dietary MAC intake; limitations of the existing measures of the gut microbiome composition and metabolic activity; measures of SCFA exposure; and the complexities of childhood respiratory health assessment.
本综述聚焦于当前的证据，即孕期母亲的饮食和肠道细菌暴露会影响发育中的胎儿免疫系统及后代随后患哮喘的情况。第1部分探讨了农场环境暴露、抗生素、益生元和益生菌补充剂，这些共同表明了细菌接触在免疫编程和后代哮喘中的重要性。第2部分概述了解释这些关联的拟议机制，包括胎儿 - 胎盘单位的细菌接触；肠道细菌成分与免疫球蛋白相关的经胎盘转运；产生母胎免疫协调的细胞因子信号传导；以及肠道细菌产生的免疫编程代谢产物。第3部分着重于饮食、肠道细菌和细菌代谢产物之间的相互作用。母亲的饮食会影响粪便细菌组成，饮食中可被微生物利用的碳水化合物（MACs）会选择产生短链脂肪酸（SCFAs）的细菌。来自小鼠模型的当前证据表明，母亲饮食中MACs增加、孕期SCFA暴露与后代哮喘减少之间存在关联，这至少部分是由胎儿肺部调节性T淋巴细胞的诱导介导的。第4部分讨论了未来研究的考虑因素，这些研究旨在探究母亲饮食 - 微生物组对后代哮喘的决定因素，包括测量饮食中MAC摄入量面临的挑战；肠道微生物组组成和代谢活性现有测量方法的局限性；SCFA暴露的测量方法；以及儿童呼吸健康评估的复杂性。
