The maternal microbiota drives early postnatal innate immune development

被引:852
作者
de Agueero, Mercedes Gomez [1 ]
Ganal-Vonarburg, Stephanie C. [1 ]
Fuhrer, Tobias [2 ]
Rupp, Sandra [1 ]
Uchimura, Yasuhiro [1 ]
Li, Hai [1 ]
Steinert, Anna [1 ]
Heikenwalder, Mathias [3 ]
Hapfelmeier, Siegfried [4 ]
Sauer, Uwe [2 ]
McCoy, Kathy D. [1 ]
Macpherson, Andrew J. [1 ]
机构
[1] Univ Bern, Maurice Muller Labs DKF, Univ Klin Viszerale Chirurg & Med, Inselspital, Murtenstr 35, CH-3010 Bern, Switzerland
[2] Swiss Fed Inst Technol, Inst Mol Syst Biol, CH-8093 Zurich, Switzerland
[3] German Canc Res Ctr, Div Chron Inflammat & Canc, Heidelberg, Germany
[4] Univ Bern, Inst Infect Dis, CH-3010 Bern, Switzerland
基金
欧洲研究理事会; 美国国家卫生研究院;
关键词
ARYL-HYDROCARBON RECEPTOR; ROR-GAMMA-T; DENDRITIC CELLS; LYMPHOID-CELLS; EARLY-LIFE; REVEALS; GUT; IGA; DIFFERENTIATION; COLONIZATION;
D O I
10.1126/science.aad2571
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Postnatal colonization of the body with microbes is assumed to be the main stimulus to postnatal immune development. By transiently colonizing pregnant female mice, we show that the maternal microbiota shapes the immune system of the offspring. Gestational colonization increases intestinal group 3 innate lymphoid cells and F4/80(+)CD11c(+) mononuclear cells in the pups. Maternal colonization reprograms intestinal transcriptional profiles of the offspring, including increased expression of genes encoding epithelial antibacterial peptides and metabolism of microbial molecules. Some of these effects are dependent on maternal antibodies that potentially retain microbial molecules and transmit them to the offspring during pregnancy and in milk. Pups born to mothers transiently colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.
引用
收藏
页码:1296 / 1301
页数:6
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