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Updated: Jun 29, 2025
Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Porphyromonas gingivalis infection alters microRNA composition in extracellular vesicles
Kayo Yoshida1, Kaya Yoshida1, Yasuhiro Mouri2
1Department of Oral Healthcare Promotion, Tokushima University Graduate School of Biomedical Sciences, 3-18-15, Kuramoto, Tokushima, 770-8504, Japan.
Objectives:
Periodontitis, commonly associated with Porphyromonas gingivalis (Pg), involves intricate alterations of oral intercellular interactions, in which extracellular vesicles (EVs) play a pivotal role. The understanding of the miRNA profiles in the EVs derived from Pg-infected cells (Pg-EVs) remains incomplete despite acknowledging their importance in intercellular communication during periodontitis. Therefore, our objective was to identify and characterize the miRNAs enriched in Pg-EVs.
Methods:
Microarray analysis was conducted to examine the miRNA profiles in the EVs derived from Pg-infected THP-1 cells. We compared the identified miRNAs with those upregulated in the EVs after stimulation with LPS. Additionally, we explored how inhibiting TLR signaling during Pg infection affects the transcription of specific miRNAs. We investigated the unique sequence motifs specific to the miRNAs concentrated in Pg-EVs.
Results:
The levels of eleven miRNAs, including miR-155, were increased in Pg-EVs compared with those elevated after LPS stimulation. The Pg-induced miR-155 upregulation via TLR2 but not TLR4 signaling suggests the influence of TLR signaling on the miRNA composition of EVs. Furthermore, the miRNAs upregulated in Pg-EVs contained AGAGGG and GRGGSGC sequence motifs.
Conclusions:
Our findings demonstrate that Pg-induced alterations in EV-containing miRNA composition occur in a TLR4-independent manner. Notably, the concentrated miRNAs in Pg-EVs harbor specific motifs with a high G + C content within their sequences. The upregulation of specific miRNAs in EVs under infectious conditions suggests the influence of both innate immune receptor signals and miRNA sequence characteristics.
Insights
Porphyromonas gingivalis (Pg) infection alters extracellular vesicle (EV) microRNA (miRNA) profiles, with specific sequence motifs influencing enrichment. This suggests innate immune signals and miRNA characteristics regulate EV communication in periodontitis.
Area of Science:
- Oral microbiology and immunology
- Extracellular vesicle research
- MicroRNA biology
Background:
- Periodontitis, often caused by Porphyromonas gingivalis (Pg), involves complex changes in oral cell interactions.
- Extracellular vesicles (EVs) are key mediators of intercellular communication in periodontitis.
- The specific microRNA (miRNA) content of EVs in Pg-infected cells is not fully understood.
Purpose of the Study:
- To identify and characterize miRNAs enriched in EVs derived from Pg-infected cells (Pg-EVs).
- To understand the role of Toll-like receptor (TLR) signaling in miRNA enrichment within Pg-EVs.
- To investigate sequence motifs characteristic of miRNAs concentrated in Pg-EVs.
Main Methods:
- Microarray analysis of miRNA profiles in EVs from Pg-infected THP-1 cells.
- Comparison of miRNA levels in Pg-EVs versus EVs stimulated with lipopolysaccharide (LPS).
- Assessment of TLR signaling inhibition effects on miRNA transcription and investigation of miRNA sequence motifs.
Main Results:
- Eleven miRNAs, including miR-155, were significantly increased in Pg-EVs compared to LPS-stimulated EVs.
- Pg-induced miR-155 upregulation occurred via TLR2, but not TLR4, signaling.
- Enriched miRNAs in Pg-EVs contained specific sequence motifs, such as AGAGGG and GRGGSGC, with high G+C content.
Conclusions:
- Pg infection alters EV miRNA composition independently of TLR4 signaling.
- Specific sequence motifs, particularly those with high G+C content, are associated with miRNA enrichment in Pg-EVs.
- Both innate immune receptor signaling and intrinsic miRNA sequence features likely regulate EV miRNA composition during infection.
