RT Journal Article
SR Electronic
T1 Gut dysbiosis induces the development of pre-eclampsia through bacterial translocation
JF Gut
JO Gut
FD BMJ Publishing Group Ltd and British Society of Gastroenterology
SP 513
OP 522
DO 10.1136/gutjnl-2019-319101
VO 69
IS 3
A1 Xia Chen
A1 Pan Li
A1 Mian Liu
A1 Huimin Zheng
A1 Yan He
A1 Mu-Xuan Chen
A1 Wenli Tang
A1 Xiaojing Yue
A1 Yongxin Huang
A1 Lingling Zhuang
A1 Zhijian Wang
A1 Mei Zhong
A1 Guibao Ke
A1 Haoyue Hu
A1 Yinglin Feng
A1 Yun Chen
A1 Yanhong Yu
A1 Hongwei Zhou
A1 Liping Huang
YR 2020
UL http://gut.bmj.com/content/69/3/513.abstract
AB Objective Pre-eclampsia (PE) is one of the malignant metabolic diseases that complicate pregnancy. Gut dysbiosis has been identified for causing metabolic diseases, but the role of gut microbiome in the pathogenesis of PE remains unknown.Design We performed a case–control study to compare the faecal microbiome of PE and normotensive pregnant women by 16S ribosomal RNA (rRNA) sequencing. To address the causative relationship between gut dysbiosis and PE, we used faecal microbiota transplantation (FMT) in an antibiotic-treated mouse model. Finally, we determined the microbiome translocation and immune responses in human and mouse placental samples by 16S rRNA sequencing, quantitative PCR and in situ hybridisation.Results Patients with PE showed reduced bacterial diversity with obvious dysbiosis. Opportunistic pathogens, particularly Fusobacterium and Veillonella, were enriched, whereas beneficial bacteria, including Faecalibacterium and Akkermansia, were markedly depleted in the PE group. The abundances of these discriminative bacteria were correlated with blood pressure (BP), proteinuria, aminotransferase and creatinine levels. On successful colonisation, the gut microbiome from patients with PE triggered a dramatic, increased pregestational BP of recipient mice, which further increased after gestation. In addition, the PE-transplanted group showed increased proteinuria, embryonic resorption and lower fetal and placental weights. Their T regulatory/helper-17 balance in the small intestine and spleen was disturbed with more severe intestinal leakage. In the placenta of both patients with PE and PE-FMT mice, the total bacteria, Fusobacterium, and inflammatory cytokine levels were significantly increased.Conclusions This study suggests that the gut microbiome of patients with PE is dysbiotic and contributes to disease pathogenesis.