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Porphyromonas gingivalis-derived lipopolysaccharide causes excessive hepatic lipid accumulation via activating NF-kappa B and JNK signaling pathways

文献类型：期刊论文

作者Ding, Lu-yang2; Liang, Li-zong3; Yang, Ya-nan3; Luo, Li-jun3; Zhao, Yong-xu1; Liu, Feng1; Ding, Qiu-rong1; ,
刊名ORAL DISEASES
出版日期2019
卷号25期号:7页码:1789-1797
关键词JNK NF-kappa B non-alcoholic fatty liver disease periodontitis Porphyromonas gingivalis
ISSN号1354-523X
DOI10.1111/odi.13153
文献子类Article
英文摘要Background Porphyromonas gingivalis is the main pathogen of periodontal disease affecting over half of the worldwide adult population. Recent studies have shown that P. gingivalis is related to the development of non-alcoholic fatty liver disease (NAFLD), a global major chronic liver disease, especially in developed countries. However, how P. gingivalis contributes to the pathogenesis of NAFLD has not been fully clarified. We aimed to conduct a preliminary exploration of the underlying mechanism of P. gingivalis infection in the development of NAFLD. Methods Human hepatocellular cells HepG2 were incubated with/without oleic acid (OA) and tested for lipid accumulation upon stimulation by lipopolysaccharide (LPS) derived from P. gingivalis or Escherichia coli. Intracellular lipid droplet formation was analyzed and quantified by Oil Red O staining. The involvement of signaling pathway molecules and pro-inflammatory cytokines related to NF-kappa B and MAPKs were examined with Western blot and quantitative real-time PCR (qRT-PCR) analyses and further evaluated with inhibitor treatment and RNA interference. Results HepG2 cells accumulated more intracellular lipids when stimulated with P. gingivalis LPS, as compared to cells treated with E. coli LPS or control. Further pathway analysis demonstrated that after stimulation with P. gingivalis LPS, cells displayed significantly upregulated MyD88 expression, increased phosphorylation of p65 and JNK, and more release of pro-inflammatory cytokines, such as IL-1, IL-8, and TNF-alpha. In addition, suppression of phosphorylation of p65 and JNK by inhibitors and RNA interference resulted in a reduction in lipid accumulation upon P. gingivalis LPS treatment. Conclusions These results suggest that P. gingivalis-derived LPS may contribute to intracellular lipid accumulation and inflammatory reaction of HepG2 cells via the activation of NF-kappa B and JNK signaling pathways. This study offers a possible explanation to the functional involvement of P. gingivalis infection in the pathological progression of NAFLD. These findings may help design new treatment strategies in NAFLD.
学科主题Dentistry, Oral Surgery & Medicine
WOS关键词FATTY LIVER-DISEASE ; STEATOHEPATITIS ; EXPRESSION ; STRESS ; TRANSDUCTION ; PATHOGENESIS ; LIPOPROTEIN ; PREVALENCE ; PATHOLOGY ; OBESITY
语种英语
WOS记录号WOS:000478508100001
出版者WILEY
版本出版稿
源URL[http://202.127.25.144/handle/331004/540]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Nutr & Hlth, Shanghai Inst Biol Sci,CAS Key Lab Nutr Metab & F, Shanghai 200031, Peoples R China,
2.Weifang Med Univ, Sch Stomatol, Weifang, Peoples R China;
3.Tongji Univ, Shanghai Engn Res Ctr Tooth Restorat & Regenerat, Sch Stomatol, Dept Periodont, Shanghai 200072, Peoples R China;
推荐引用方式
GB/T 7714		 Ding, Lu-yang,Liang, Li-zong,Yang, Ya-nan,et al. Porphyromonas gingivalis-derived lipopolysaccharide causes excessive hepatic lipid accumulation via activating NF-kappa B and JNK signaling pathways[J]. ORAL DISEASES,2019,25(7):1789-1797.
APA Ding, Lu-yang.,Liang, Li-zong.,Yang, Ya-nan.,Luo, Li-jun.,Zhao, Yong-xu.,...&,.(2019).Porphyromonas gingivalis-derived lipopolysaccharide causes excessive hepatic lipid accumulation via activating NF-kappa B and JNK signaling pathways.ORAL DISEASES,25(7),1789-1797.
MLA Ding, Lu-yang,et al."Porphyromonas gingivalis-derived lipopolysaccharide causes excessive hepatic lipid accumulation via activating NF-kappa B and JNK signaling pathways".ORAL DISEASES 25.7(2019):1789-1797.

入库方式： OAI收割

来源：上海营养与健康研究所

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