ArticleNPJ biofilms and microbiomes2024
Clostridium difficile-derived membrane vesicles promote fetal growth restriction via inhibiting trophoblast motility through PPARγ/RXRα/ANGPTL4 axis.
Article in NPJ biofilms and microbiomes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Host metabolism shapes the intestinal microbiota: a top-down paradigm of environmental selection pressure.Gut microbes · 2026Review
- Review
- Sub-inhibitory concentrations of metronidazole alter the proteomic profile and biological effects of extracellular vesicles from Clostridioides difficile.BMC microbiology · 2026Article
- Clostridioides difficile-Derived Extracellular Vesicles Induce Proinflammatory Responses in Macrophages.Journal of extracellular vesicles · 2026Article
- Combined PDGF and ANGPTL4 in diabetic foot: diagnostic value and exploratory early changes after plantar arch angioplasty plus alprostadil.American journal of translational research · 2026Article
- Cytoplasmic membrane vesicles fromFrontiers in microbiology · 2026Article
- Extracellular DNA filaments associated with surface polysaccharide II give Clostridioides difficile biofilm matrix a network-like structure.NPJ biofilms and microbiomes · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Fetal growth restriction (FGR) is a common complication of pregnancy, which seriously endangers fetal health and still lacks effective therapeutic targets. Clostridium difficile (C. difficile) is associated with fetal birth weight, and its membrane vesicles (MVs) are pathogenic vectors. However, the role of C. difficile and its MVs in FGR remains unclear. Here we found that supplementation with C. difficile altered the characteristics of gut microbiota and reduced the birth weight in mice. Interestingly, C. difficile MVs entered placenta, inhibited trophoblast motility, and induced fetal weight loss in mice. Mechanistically, C. difficile MVs activated the PPAR pathway via enhancing the transcriptional activity of PPARγ promoter, consequently inhibiting trophoblast motility. Moreover, PPARγ expression was significantly elevated in FGR placenta, and negatively correlated with fetal birth weight. Together, our findings reveal the significance of C. difficile and its MVs in FGR, providing new insights into the mechanisms of FGR development.
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