小柯机器人

澳大利亚昆士兰大学Simon Phipps研究小组发现，母体饮食调节婴儿微生物群和树突状细胞发育及呼吸道感染免疫所需的肠道Flt3L。相关论文于2023年3月31日在线发表于国际学术期刊《免疫》。

研究人员证明了在小鼠中，由于浆细胞树突状细胞（pDC）的招募延迟和肺部调节性T细胞扩张的干扰，母体低纤维饮食（LFD）导致婴儿下呼吸道感染（LRI）的严重性增强。LFD改变了母体乳汁微生物组的组成和婴儿肠道微生物组的集合。这些微生物的变化减少了新生儿肠道上皮细胞对DC生长因子Flt3L的分泌，并损害了下游pDC的造血功能。用从高纤维饮食母亲的乳汁中分离出的丙酸盐生产菌进行治疗，或补充丙酸盐，通过恢复肠道Flt3L的表达和pDC的造血功能，对严重下呼吸道感染（sLRI）起到保护作用。

这些研究结果发现，肠道中的微生物依赖性Flt3L轴在生命早期促进pDC造血并赋予对sLRI的疾病抵抗力。

据介绍，怀孕期间母体饮食不良是后代sLRI的一个风险因素，但其潜在机制仍然难以捉摸。

附：英文原文

Title: Maternal diet modulates the infant microbiome and intestinal Flt3L necessary for dendritic cell development and immunity to respiratory infection

Author: Md. Al Amin Sikder, Ridwan B. Rashid, Tufael Ahmed, Ismail Sebina, Daniel R. Howard, Md. Ashik Ullah, Muhammed Mahfuzur Rahman, Jason P. Lynch, Bodie Curren, Rhiannon B. Werder, Jennifer Simpson, Alec Bissell, Mark Morrison, Carina Walpole, Kristen J. Radford, Vinod Kumar, Trent M. Woodruff, Tan Hui Ying, Ayesha Ali, Gerard E. Kaiko, John W. Upham, Robert D. Hoelzle, Páraic ó. Cuív, Patrick G. Holt, Paul G. Dennis, Simon Phipps

Issue&Volume: 2023-03-31

Abstract: Poor maternal diet during pregnancy is a risk factor for severe lower respiratoryinfections (sLRIs) in the offspring, but the underlying mechanisms remain elusive.Here, we demonstrate that in mice a maternal low-fiber diet (LFD) led to enhancedLRI severity in infants because of delayed plasmacytoid dendritic cell (pDC) recruitmentand perturbation of regulatory T cell expansion in the lungs. LFD altered the compositionof the maternal milk microbiome and assembling infant gut microbiome. These microbialchanges reduced the secretion of the DC growth factor Flt3L by neonatal intestinalepithelial cells and impaired downstream pDC hematopoiesis. Therapy with a propionate-producingbacteria isolated from the milk of high-fiber diet-fed mothers, or supplementationwith propionate, conferred protection against sLRI by restoring gut Flt3L expressionand pDC hematopoiesis. Our findings identify a microbiome-dependent Flt3L axis inthe gut that promotes pDC hematopoiesis in early life and confers disease resistanceagainst sLRIs.

DOI: 10.1016/j.immuni.2023.03.002

Source: https://www.cell.com/immunity/fulltext/S1074-7613(23)00119-X

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