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Updated: Sep 18, 2025
Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages
Published on: February 22, 2017
Veillonella parvula outer membrane vesicles increase ICAM-1+ neutrophils exhibiting elevated NET formation via
Lina Xu1, Yiting Jiang1, Xuri Zhao2
1Department of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai, China.
Background:
Veillonella parvula (V. parvula), as an anaerobic Gram-negative coccus, produces outer membrane vesicles (OMVs) to promote bacterial colonization and periodontitis progress. Neutrophils are the first immune cells during bacterial stimulation, while neutrophil extracellular traps (NETs) are the early triggers in the progress of periodontitis. However, the interactions between neutrophils and V. parvula are still unknown. Therefore, this study investigated the effects and underlying mechanisms of V. parvula OMVs on neutrophils.
Methods:
Neutrophil migration, apoptosis, and phagocytosis and reactive oxygen species (ROS) production were assessed following stimulation with V. parvula OMVs. The differential gene expression in neutrophils was characterized using RNA sequencing. The correlation between intercellular adhesion molecule 1 (ICAM-1) expression and NET formation was verified through flow cytometry and immunofluorescence. The NET formation-associated components, including cell-free DNA, neutrophil elastase, myeloperoxidase, and the PAD4 expression were analyzed. The frequencies of the ICAM-1+ neutrophils and NET formation were evaluated in neutrophils pretreated with CYBB or PAD4 inhibitors.
Results:
Neutrophils exhibited robust migration, increased apoptosis, and ROS production following exposure to V. parvula OMVs. No significant differences were observed in neutrophil phagocytosis. RNA sequencing analysis revealed a significant increase in the expression of Icam-1 mRNA. And higher ICAM-1+ neutrophils in the V. parvula OMVs group enhanced the levels of NET formation via activation of ROS-PAD4 signaling pathway.
Conclusions:
V. parvula OMVs were initially found to increase the population of ICAM-1+ neutrophils, which subsequently exhibited elevated NET formation via the ROS-PAD4 signaling pathway. This study elucidates a novel pathogenic mechanism of V. parvula OMVs and highlights the potential of targeting ICAM-1+ neutrophils as a therapeutic approach for chronic periodontitis.
Insights
Veillonella parvula outer membrane vesicles (OMVs) increase neutrophil migration, apoptosis, and ROS production. These OMVs promote NET formation via ICAM-1+ neutrophils and the ROS-PAD4 pathway, offering a therapeutic target for periodontitis.
Area of Science:
- Microbiology
- Immunology
- Periodontology
Background:
- Veillonella parvula (V. parvula) produces outer membrane vesicles (OMVs) that contribute to periodontitis.
- Neutrophils and their extracellular traps (NETs) are critical in early periodontitis, but their interaction with V. parvula is unclear.
Purpose of the Study:
- To investigate the effects of V. parvula OMVs on neutrophils.
- To elucidate the underlying mechanisms of V. parvula OMVs in neutrophil activation and NET formation.
Main Methods:
- Assessed neutrophil migration, apoptosis, phagocytosis, and reactive oxygen species (ROS) production after V. parvula OMV stimulation.
- Utilized RNA sequencing for differential gene expression analysis.
- Verified the correlation between intercellular adhesion molecule 1 (ICAM-1) and NET formation using flow cytometry and immunofluorescence, analyzing NET components and PAD4 expression.
Main Results:
- V. parvula OMVs induced neutrophil migration, apoptosis, and ROS production, but not altered phagocytosis.
- RNA sequencing revealed increased ICAM-1 mRNA expression.
- Elevated ICAM-1+ neutrophils enhanced NET formation through ROS-PAD4 signaling.
Conclusions:
- V. parvula OMVs increase ICAM-1+ neutrophils, which subsequently enhance NET formation via the ROS-PAD4 pathway.
- This study reveals a novel pathogenic mechanism of V. parvula OMVs.
- Targeting ICAM-1+ neutrophils presents a potential therapeutic strategy for chronic periodontitis.
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