Preeclampsia, the presence of hypertension and dysfunction in one or more maternal organ systems, is a common pregnancy complication. Late-onset preeclampsia, which occurs after 34 weeks, is linked to metabolic and immune dysfunction. It is unclear if the altered composition of the gut microbiota in overt preeclampsia occurs prior to symptom development. Altered gut microbiota composition may reduce gut wall integrity, which increases the transfer of inflammatory molecules into the host or through reduced secretion of beneficial metabolites to the host. This study aims to investigate if changes to the gut microbiota occur before symptoms.
Ten participants in the Study of PRobiotics IN the prevention of GDM (SPRING), who developed late-onset preeclampsia (DPE) were matched with 24 participants who remained normotensive throughout pregnancy (C). Stool samples were collected at 28 weeks gestation and subjected to metagenomic sequencing. Metagenome assembled genomes were collected and combined with the Unified Human Gastrointestinal Genome collection and used for taxonomic assignment. Metagenome sequences were also mapped to the UniRef90 database and assigned to MetaCyc metabolic pathways.
The beta diversity of the gut microbiota in DPE women was significantly different from the C group (P=0.0024), with no differences in richness or evenness (alpha diversity) between the groups. DPE women demonstrated an enrichment of 61 species, particularly multiple members of the Enterocloster and Blautia genera but depletion of 33 species including multiple members of the Collinsella and the short-chain fatty acid-producing Faecalibacterium genera. Metabolically, 14 pathways were enriched in DPE women, including the glycosaminoglycan degradation pathway.
Our results indicate that there are changes to the gut microbiota composition in DPE women. Increased glycosaminoglycan degradation of the extracellular matrix components of the gut wall could contribute to decreased gut wall integrity and thereby increase inflammatory signalling in the mother thereby contributing to the development of symptoms.