Lipid droplets affect elimination of Porphyromonas gingivalis in HepG2 cells by altering the autophagy-lysosome system

Zaitsu, Yumi; Iwatake, Mayumi; Satô, Keiko; Tsukuba, Takayuki

doi:10.1016/j.micinf.2016.05.004

Cited by 18 publications

(15 citation statements)

References 22 publications

(28 reference statements)

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“…196 In addition, a P. gingivalis trypsin-like gingipain enzyme is translocated to mouse liver with the outer membrane vesicles of P. gingivalis and it suppresses Akt/glycogen synthase kinase 3 beta signaling, resulting in attenuation of hepatic glycogen synthesis with hyperglycemia in response to insulin. 197 Using an in vitro model of nonalcoholic fatty liver disease that is mediated by treating HepG2 cells with oleic acid, Zaitsu et al 198 found that intracellular lipid droplets suppress the elimination of P. gingivalis from hepatic cells by altering lysosome formation and autophagy at an early phase of infection.…”

Section: Periodontopathic Bacteriamentioning

confidence: 99%

Periodontal disease–related nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: An emerging concept of oral‐liver axis

Kuraji

Sekino

Kapila

et al. 2021

Periodontology 2000

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Periodontal disease is a common chronic inflammatory and infectious disease that is caused by an oral biofilm-mediated microbial dysbiosis that is predominantly comprised of anaerobic gram-negative bacteria, namely periodontopathic bacteria. 1,2 These biofilms are a continually renewing storehouse of lipopolysaccharide and other microbial molecules that are derived from the resident gram-negative bacteria. Biofilm components have ready access to the periodontal tissues and host circulation. Microbial challengesThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Section: Periodontopathic Bacteriamentioning

confidence: 99%

Periodontal disease–related nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: An emerging concept of oral‐liver axis

Kuraji

Sekino

Kapila

et al. 2021

Periodontology 2000

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“…Studies have found that P. gingivalis can internalize in a variety of host cells and is closely related to the occurrence and development of a variety of systemic diseases (Gibson et al, 2004 ; Kozarov et al, 2005 ; Karnoutsos et al, 2008 ; Zaitsu et al, 2016 ). Therefore, antagonizing P. gingivalis in host cells is helpful to control periodontitis and systemic diseases.…”

Section: Discussionmentioning

confidence: 99%

LL-37-Induced Autophagy Contributed to the Elimination of Live Porphyromonas gingivalis Internalized in Keratinocytes

Yang

Niu

Pan

et al. 2020

Front. Cell. Infect. Microbiol.

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Porphyromonas gingivalis (P. gingivalis), one of the most important pathogens of periodontitis, is closely associated with the aggravation and recurrence of periodontitis and systemic diseases. Antibacterial peptide LL-37, transcribed from the cathelicidin antimicrobial peptide (CAMP) gene, exhibits a broad spectrum of antibacterial activity and regulates the immune system. In this study, we demonstrated that LL-37 reduced the number of live P. gingivalis (ATCC 33277) in HaCaT cells in a dose-dependent manner via an antibiotic-protection assay. LL-37 promoted autophagy of HaCaT cells internalized with P. gingivalis. Inhibition of autophagy with 3-methyladenine (3-MA) weakened the inhibitory effect of LL-37 on the number of intracellular P. gingivalis. A cluster of orthologous groups (COGs) and a gene ontology (GO) functional analysis were used to individually assign 65 (10%) differentially expressed genes (DEGs) to an "Intracellular trafficking, secretion, and vesicular transport" cluster and 306 (47.08%) DEGs to metabolic processes including autophagy. Autophagy-related genes, a tripartite motif-containing 22 (TRIM22), and lysosomal-associated membrane protein 3 (LAMP3) were identified as potentially involved in LL-37-induced autophagy. Finally, bioinformatics software was utilized to construct and predict the protein-protein interaction (PPI) network of CAMP-TRIM22/LAMP3-Autophagy. The findings indicated that LL-37 can reduce the quantity of live P. gingivalis internalized in HaCaT cells by promoting autophagy in these cells. The transcriptome sequencing and analysis also revealed the potential molecular pathway of LL-37-induced autophagy.

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“…It is widely regarded as being the hepatic manifestation of conditions related to metabolic syndromes [171], including type 2 diabetes, insulin resistance, obesity, hyperlipidemia, hypertriglyceridemia, and hypertension. Studies on mice [172] revealed that infection with P. gingivalis promoted the pathological progression of NAFLD. Internalized P. gingivalis was localized in autophagosomes and lysosomes in HepG2 cells, rather than in liquid droplets.…”

Section: P Gingivalis In the Digestive Systemmentioning

confidence: 99%

Porphyromonas gingivalis outside the oral cavity

et al. 2021

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HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

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Lipid droplets affect elimination of Porphyromonas gingivalis in HepG2 cells by altering the autophagy-lysosome system

Cited by 18 publications

References 22 publications

Periodontal disease–related nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: An emerging concept of oral‐liver axis

Periodontal disease–related nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: An emerging concept of oral‐liver axis

LL-37-Induced Autophagy Contributed to the Elimination of Live Porphyromonas gingivalis Internalized in Keratinocytes

Porphyromonas gingivalis outside the oral cavity

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