Extracellular vesicles from periodontal pathogens regulate hepatic steatosis via Toll‐like receptor 2 and plasminogen activator inhibitor‐1

Author:

Kim Hyun Young12,Lim Younggap1,Jang Ji Sun3,Ko Yeon Kyeong4,Choi Youngnim42,Kim Hong‐Hee32,Choi Bong‐Kyu1ORCID

Affiliation:

1. Department of Oral Microbiology and Immunology School of Dentistry Seoul National University Seoul Republic of Korea

2. Dental Research Institute School of Dentistry Seoul National University Seoul Republic of Korea

3. Department of Cell and Developmental Biology School of Dentistry Seoul National University Seoul Republic of Korea

4. Department of Immunology and Molecular Microbiology School of Dentistry Seoul National University Seoul Republic of Korea

Abstract

AbstractPlasminogen activator inhibitor‐1 (PAI‐1) is associated with nonalcoholic fatty liver disease (NAFLD) by lipid accumulation in the liver. In this study, we showed that extracellular vesicles (EVs) from the periodontal pathogens Filifactor alocis and Porphyromonas gingivalis induced steatosis by inducing PAI‐1 in the liver and serum of mice fed a low‐fat diet. PAI‐1 induction was not observed in TLR2−/− mice. When tested using HEK‐Blue hTLR2 cells, human TLR2 reporter cells, the TLR2‐activating ability of serum from NAFLD patients (n = 100) was significantly higher than that of serum from healthy subjects (n = 100). Correlation analysis confirmed that PAI‐1 levels were positively correlated with the TLR2‐activating ability of serum from NAFLD patients and healthy subjects. Amphiphilic molecules in EVs were involved in PAI‐1 induction. Our data demonstrate that the TLR2/PAI‐1 axis is important for hepatic steatosis by EVs of periodontal pathogens.

Publisher

Wiley

Subject

Cell Biology,Histology

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