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Updated: Mar 18, 2026
Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva
Published on: April 3, 2018
Porphyromonas gingivalis-induced miR-132 regulates TNFα expression in THP-1 derived macrophages
Mi Hee Park1, Eunjoo Park1, Hyung-Joon Kim2
1Department of Oral Microbiology, School of Dentistry, Pusan National University, Yangsan-si, Gyeongsangnam-do 626-870 South Korea.
Background:
Periodontitis is a chronic inflammatory disease induced by periodontopathogens such as Porphyromonas gingivalis (P. gingivalis). MicroRNAs (miRNAs) are small single-stranded noncoding RNAs that regulate gene expression at the level of translation. MiRNAs have been reported to be involved in inflammatory processes. In this study, we examined the effects of P. gingivalis-induced inflammatory miRNAs expression on TNFα production in THP-1 derived macrophages.
Results:
Porphyromonas gingivalis induced the expression of miR-132. P. gingivalis-induced miR-132 expression was significantly inhibited by TLR2/4 knock-down and NF-κB inhibitor. Additionally, miR-132 antagomir strongly repressed production of TNFα. The expression of NFE2L2 and NFAT5, the putative target genes of miR-132 involved in regulation of TNFα, decreased in response to P. gingivalis. Furthermore, miR-132 antagomir rescued P. gingivalis-induced suppression of NFE2L2 and NFAT5.
Conclusions:
These results suggest that the induction of miR-132 by P. gingivalis can modulate the pathogenesis of periodontitis induced via regulatory expression of TNFα.
Insights
Porphyromonas gingivalis infection increases miR-132, a microRNA that promotes periodontitis by boosting TNFα. Inhibiting miR-132 reduces TNFα and may offer a therapeutic strategy for periodontitis.
Area of Science:
- Microbiology
- Molecular Biology
- Immunology
Background:
- Periodontitis is a chronic inflammatory disease caused by bacteria like Porphyromonas gingivalis.
- MicroRNAs (miRNAs) are key regulators of gene expression involved in inflammation.
Purpose of the Study:
- To investigate the role of P. gingivalis-induced miRNAs in TNFα production in macrophages.
- To explore the regulatory pathway involving miR-132 and its targets in periodontitis.
Main Methods:
- THP-1 derived macrophages were treated with P. gingivalis.
- Expression levels of miR-132 and target genes (NFE2L2, NFAT5) were analyzed.
- TLR2/4 knock-down and NF-κB inhibition were employed.
- miR-132 antagomir was used to assess its effect on TNFα production and target gene expression.
Main Results:
- P. gingivalis significantly induced miR-132 expression.
- This induction was dependent on TLR2/4 signaling and NF-κB activation.
- Inhibition of miR-132 using an antagomir suppressed TNFα production.
- P. gingivalis decreased NFE2L2 and NFAT5 expression, which was reversed by miR-132 antagomir.
Conclusions:
- P. gingivalis-induced miR-132 plays a critical role in modulating TNFα production during periodontitis.
- miR-132 may be a potential therapeutic target for managing periodontitis pathogenesis.
