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Effects and Mechanisms of Porphyromonas Gingivalis Outer Membrane Vesicles Induced Cardiovascular Injury

Overview
Journal BMC Oral Health
Publisher Biomed Central
Specialty Dentistry
Date 2024 Jan 19
PMID 38243239
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Abstract

Background: The outer membrane vesicles (OMVs) derived from Porphyromonas gingivalis (P. gingivalis) have long been acknowledged for their crucial role in the initiation of periodontitis. However, the implications of P. gingivalis OMVs in the context of cardiovascular disease (CVD) remain incompletely understood. This study aimed to clarify both the impact and the underlying mechanisms through which P. gingivalis OMVs contribute to the propagation of distal cardiovascular inflammation and trauma.

Methods: In this study, various concentrations (0, 1.25, 2.5, and 4.5 µg/µL) of P. gingivalis OMVs were microinjected into the common cardinal vein of zebrafish larvae at 48 h post-fertilization (hpf) to assess changes in cardiovascular injury and inflammatory response. Zebrafish larvae from both the PBS and the 2.5 µg/µL injection cohorts were harvested at 30 h post-injection (hpi) for transcriptional analysis. Real-time quantitative PCR (RT-qPCR) was employed to evaluate relative gene expression.

Results: These findings demonstrated that P. gingivalis OMVs induced pericardial enlargement in zebrafish larvae, caused vascular damage, increased neutrophil counts, and activated inflammatory pathways. Transcriptomic analysis further revealed the involvement of the immune response and the extracellular matrix (ECM)-receptor interaction signaling pathway in this process.

Conclusion: This study illuminated potential mechanisms through which P. gingivalis OMVs contribute to CVD. It accentuated their involvement in distal cardiovascular inflammation and emphasizes the need for further research to comprehensively grasp the connection between periodontitis and CVD.

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References
1.
Li Y, Jia Z, Zhang S, He X . Progress in Gene-Editing Technology of Zebrafish. Biomolecules. 2021; 11(9). PMC: 8468279. DOI: 10.3390/biom11091300. View

2.
Silvestre-Roig C, Braster Q, Ortega-Gomez A, Soehnlein O . Neutrophils as regulators of cardiovascular inflammation. Nat Rev Cardiol. 2020; 17(6):327-340. DOI: 10.1038/s41569-019-0326-7. View

3.
Little C, Rongish B . The extracellular matrix during heart development. Experientia. 1995; 51(9-10):873-82. DOI: 10.1007/BF01921738. View

4.
Romandini M, Baima G, Antonoglou G, Bueno J, Figuero E, Sanz M . Periodontitis, Edentulism, and Risk of Mortality: A Systematic Review with Meta-analyses. J Dent Res. 2020; 100(1):37-49. DOI: 10.1177/0022034520952401. View

5.
Bloksgaard M, Lindsey M, Martinez-Lemus L . Extracellular matrix in cardiovascular pathophysiology. Am J Physiol Heart Circ Physiol. 2018; 315(6):H1687-H1690. PMC: 6336969. DOI: 10.1152/ajpheart.00631.2018. View