{"title":"Effects of Porphyromonas gingivalis-derived lipopolysaccharide on the barrier function of cultured junctional epithelial cells","authors":"Ryo Aizawa , Masaru Sunaga , Keisuke Tanaka , Marika Sugano , Daisuke Saito , Koki Okada , Junichi Tanaka , Kenji Mishima , Matsuo Yamamoto","doi":"10.1016/j.job.2025.100721","DOIUrl":null,"url":null,"abstract":"<div><h3>Objectives</h3><div>The junctional epithelium (JE) plays an important role in maintaining the protective integrity of periodontal tissues by forming an epithelial barrier that impedes bacterial invasion. This study examined the effects of <em>Porphyromonas gingivalis</em> lipopolysaccharide (PG-LPS) on JE-1 cells, a mouse-derived junctional epithelial cell line.</div></div><div><h3>Methods</h3><div>JE-1 cells were exposed to PG-LPS, and the effects on cell viability, migration, gene expression, protein expression, and barrier function at various time points were evaluated according to the experimental type.</div></div><div><h3>Results</h3><div>PG-LPS (1 μg/mL) did not affect JE-1 cell viability but significantly inhibited migration. Treatment with PG-LPS upregulated inflammatory genes (<em>Il-6, Tlr2, Tlr4, Traf6</em>) and altered the expression of chemokines (increased <em>Cxcl2</em> and decreased <em>Cxcl10</em>) and protective factors (increased <em>Nfe2l2</em> and <em>Slpi</em>). Notably, 1 μg/mL of PG-LPS increased permeability and decreased adhesion molecule expression (<em>Cdh1</em> and <em>Itgb4</em>), whereas 10 μg/mL showed a non-linear response (apparent permeability [cm/s]: 0.868, 0.915, 1.416, 1.728, 1.224, and 1.176 with 0, 0.1, 0.5, 1, 5, and 10 μg/mL respectively), indicating compensatory mechanisms.</div></div><div><h3>Conclusions</h3><div>PG-LPS disrupts JE barrier function and alters its immunomodulatory properties, potentially contributing to periodontitis progression. These findings enhance our understanding of the underlying causes of periodontitis and inform targeted treatments to maintain JE defense against periodontopathogenic bacteria.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100721"},"PeriodicalIF":2.2000,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Oral Biosciences","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1349007925001100","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/12/2 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
引用次数: 0
Abstract
Objectives
The junctional epithelium (JE) plays an important role in maintaining the protective integrity of periodontal tissues by forming an epithelial barrier that impedes bacterial invasion. This study examined the effects of Porphyromonas gingivalis lipopolysaccharide (PG-LPS) on JE-1 cells, a mouse-derived junctional epithelial cell line.
Methods
JE-1 cells were exposed to PG-LPS, and the effects on cell viability, migration, gene expression, protein expression, and barrier function at various time points were evaluated according to the experimental type.
Results
PG-LPS (1 μg/mL) did not affect JE-1 cell viability but significantly inhibited migration. Treatment with PG-LPS upregulated inflammatory genes (Il-6, Tlr2, Tlr4, Traf6) and altered the expression of chemokines (increased Cxcl2 and decreased Cxcl10) and protective factors (increased Nfe2l2 and Slpi). Notably, 1 μg/mL of PG-LPS increased permeability and decreased adhesion molecule expression (Cdh1 and Itgb4), whereas 10 μg/mL showed a non-linear response (apparent permeability [cm/s]: 0.868, 0.915, 1.416, 1.728, 1.224, and 1.176 with 0, 0.1, 0.5, 1, 5, and 10 μg/mL respectively), indicating compensatory mechanisms.
Conclusions
PG-LPS disrupts JE barrier function and alters its immunomodulatory properties, potentially contributing to periodontitis progression. These findings enhance our understanding of the underlying causes of periodontitis and inform targeted treatments to maintain JE defense against periodontopathogenic bacteria.