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Gut Microbiota Dysbiosis in Preeclampsia: Mechanisms, Biomarkers, and Probiotic-Based Interventions

Yefang Zhao, Bingjie Wang, Xujing Wei and 9 more

Mediators of Inflammation · 2025

doi:10.1155/mi/3010379 (opens in a new tab)

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Abstract

Background: This study aimed to investigate the impact of fecal microbiota transplantation (FMT) on gut microbiota composition and serum inflammatory factors in a murine model. Methods: Female C57BL/6J mice ( n = 60) were divided into four groups: control (Con), negative (Neg), normal transplantation (NT), and preeclampsia transplantation (PET). The Con group received no treatment, while the Neg, NT, and PET groups were administered a triple antibiotic regimen (ampicillin, neomycin sulfate, and metronidazole) for 14 days to deplete gut microbiota. Following antibiotic treatment, FMT was performed: the NT group received fecal microbiota from healthy pregnant women and the PET group received microbiota from severe preeclampsia patients. Fecal samples and serum were collected for 16S rRNA sequencing and inflammatory factor analysis, respectively. Results: Significant differences in gut microbial composition were observed between the PET group and other groups, with enriched taxa such as Coprococcus , Bacillales , and Staphylococcus in the PET group. Conversely, taxa such as Helicobacter and Klebsiella were more abundant in the fecal microbiota of mice in the NT group. Furthermore, serum levels of lipopolysaccharide (LPS), tumor necrosis factor‐alpha (TNF‐α), and interleukin‐6 (IL‐6) were markedly elevated in the PET group compared to the control, negative, and NT groups. Transplantation with fecal bacteria from preeclampsia patients leads to significant alterations in gut microbiota composition and increased serum inflammatory factors levels in mice. Conclusion: These findings provide insights into the relationship between gut microbiota and inflammatory processes in preeclampsia and underscore the potential therapeutic implications of FMT in modulating gut microbiota dysbiosis and inflammatory responses.

Abstract licence: CC BY

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