背景:产前心理困扰和母体炎症可增加后代神经发育迟缓的风险;最近,肠道微生物群可能是这种关联的潜在机制,但在人群研究中尚未完全阐明.
方法:本研究纳入了72对完成妊娠晚期和6-8月龄婴儿神经发育评估的母婴对。通过16SrRNA测序和液相色谱-质谱分析确定母婴的肠道菌群及其短链脂肪酸(SCFA)。通过luminex液体悬浮微阵列检测妊娠晚期孕妇血液中的炎性细胞因子。
结果:这项研究发现,产前心理困扰组的婴儿的精细运动技能较差(β=-4.396,95%置信区间(CI)=-8.546,-0.246,p=0.038),与对照组相比,解决问题的能力(β=-5.198,95%CI=-10.358,-0.038,p=0.048)和总体发展能力(β=-22.303,95CI=-41.453,-3.153,p=0.022)。该研究还表明,在妊娠晚期,白细胞介素-1β(IL-1β)(β=-1.951,95CI=-3.321,-0.581,p=0.005)和干扰素诱导蛋白-10(IP-10)(β=-0.019,95CI=-0.034,-0.004,p=0.015)的水平较高,婴儿的精细运动技能较差。此外,IL-10水平较高(β=-0.498,95CI=-0.862,-0.133,p=0.007),IL-12p70(β=-0.113,95CI=-0.178,-0.048,p=0.001),IL-17A(β=-0.817,95CI=-1.517,-0.118,p=0.022),干扰素-γ(β=-0.863,95CI=-1.304,-0.422,p<0.001),IP-10(β=-0.020,95CI=-0.038,-0.001,p=0.035),并且在妊娠晚期激活正常T细胞表达和分泌(β=-0.002,95CI=-0.003,-0.001,p=0.005)时受到调节,婴儿解决问题的能力较差。在控制相关协变量后,本研究发现母亲肠道菌群Roseburia介导了产前心理困扰与婴儿总神经发育之间的关系(a=0.433,95CI=0.079,0.787,p=0.017;b=-19.835,95CI=-33.877,-5.792,p=0.006;c=22.407,95CI=-43.207,-1.608,p=0.035;间接效应=-0.584,-
结论:这是第一项强调母婴肠道菌群在产前心理困扰和婴儿神经发育中的作用的研究。需要进一步的研究来探索产前心理困扰之间关系的生物学机制。母婴肠道菌群,和婴儿神经发育。
BACKGROUND: Prenatal psychological distress and maternal inflammation can increase the risk of neurodevelopmental delay in offspring; recently, the gut microbiota has been shown to may be a potential mechanism behind this association and not fully elucidated in population study.
METHODS: Seventy-two maternal-infant pairs who completed the assessments of prenatal psychological distress during the third trimester and neurodevelopment of infants at age 6-8 months of age were included in this study. The gut microbiota and its short-chain fatty acids (SCFAs) of maternal-infant were determined by 16S rRNA sequencing and liquid chromatography-mass spectrometry analysis. Inflammatory cytokines in the blood of pregnant women during the third trimester were detected by luminex liquid suspension microarrays.
RESULTS: This study found that infants in the prenatal psychological distress group had poorer fine motor skills (β = -4.396, 95 % confidence interval (CI) = -8.546, -0.246, p = 0.038), problem-solving skills (β = -5.198, 95 % CI = -10.358, -0.038, p = 0.048) and total development (β = -22.303, 95%CI = -41.453, -3.153, p = 0.022) compared to the control group. The study also indicated that the higher level of interleukin-1β (IL-1β) (β = -1.951, 95%CI = -3.321, -0.581, p = 0.005) and interferon-inducible protein-10 (IP-10) (β = -0.019, 95%CI = -0.034, -0.004, p = 0.015) during the third trimester, the poorer fine motor skills in infants. Also, the higher level of IL-10 (β = -0.498, 95%CI = -0.862, -0.133, p = 0.007), IL-12p70 (β = -0.113, 95%CI = -0.178, -0.048, p = 0.001), IL-17 A (β = -0.817, 95%CI = -1.517, -0.118, p = 0.022), interferon-γ (β = -0.863, 95%CI = -1.304, -0.422, p < 0.001), IP-10 (β = -0.020, 95%CI = -0.038, -0.001, p = 0.035), and regulated upon activation normal T cell expressed and secreted (β = -0.002, 95%CI = -0.003, -0.001, p = 0.005) during the third trimester, the poorer problem-solving skills in infants. After controlling for relevant covariates, this study found that maternal gut microbiota Roseburia mediates the relationship between prenatal psychological distress and total neurodevelopment of infants (a = 0.433, 95%CI = 0.079, 0.787, p = 0.017; b = -19.835, 95%CI = -33.877, -5.792, p = 0.006; c = 22.407, 95%CI = -43.207,-1.608, p = 0.035; indirect effect = -8.584, 95%CI = -21.227, -0.587).
CONCLUSIONS: This is the first study to emphasize the role of the maternal-infant gut microbiota in prenatal psychological distress and infant neurodevelopment. Further studies are needed to explore the biological mechanisms underlying the relationship between prenatal psychological distress, maternal-infant gut microbiota, and infant neurodevelopment.