Related Experiment Video
Updated: Aug 5, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
Published on: January 26, 2024
Porphyromonas Gingivalis Outer Membrane Vesicles Disrupt Trophoblast Mitochondrial FAO and Drive Adverse Pregnancy
Yijia Wang1, Siyan Liu1, Jiebing Zhang2
1Laboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing 100070, China.
Abstract:
Background: Periodontitis is increasingly recognised as a significant risk factor for adverse pregnancy outcomes (APOs), yet the mechanisms by which oral pathogens trigger placental dysfunction remain unclear. Porphyromonas gingivalis (Pg), a keystone periodontal pathogen, secretes outer membrane vesicles (Pg-OMVs) that carry virulence factors and can reach distant organs. However, the impact of Pg-OMVs on placental trophoblasts and the accompanying metabolic disturbances is poorly understood. This study investigated the effects of Pg-OMVs on trophoblast function and metabolism. Methods:Pg-OMVs were isolated from Pg cultures. Pregnant mice were exposed to Pg-OMVs in vivo, and placental and uterine weights were recorded. Human trophoblast cells were treated with Pg-OMV in vitro. Untargeted metabolomic profiling of placental tissues was conducted using liquid chromatography-mass spectrometry. Fatty acid β-oxidation (FAO) activity, CD36 expression, and mitochondrial integrity were assessed via enzymatic assays, immunoblotting, transmission electron microscopy, mitochondrial membrane potential measurements, and oxygen consumption rate analysis. Results:Pg-OMVs were internalised by placental trophoblasts, and their presence was associated with significantly reduced placental and uterine weights. Metabolomics revealed a marked accumulation of long-chain acylcarnitines, particularly C20:1 carnitine, indicating impaired FAO. Pg-OMV exposure suppressed FAO activity, downregulated the fatty acid translocase CD36, and induced severe mitochondrial dysfunction, evidenced by cristae loss, decreased mitochondrial membrane potential, and diminished oxygen consumption rates. Conclusions:Pg-OMV compromise placental integrity by disrupting mitochondrial fatty acid β-oxidation, providing a novel mechanistic link between periodontal pathogen-derived vesicles and the pathogenesis of APOs.
Related Concept Videos
Development of the Oral Microbiota
Teratogenicity
Oogenesis
Structure of Porins
Trichomoniasis
Porin Insertion in the Outer Mitochondrial Membrane
Three models describe the assembly of porins by the SAM complex and their insertion into the outer membrane. Model 1 suggests that porins are assembled outside the SAM channel as the...
