<i>Porphyromonas gingivalis</i> triggers inflammation in hepatocyte depend on ferroptosis via activating the NF‐κB signaling pathway

Yao, Chao; Lan, Dongmei; Li, Xue; Wang, Yan; Qi, Shengcai

doi:10.1111/odi.14537

Cited by 4 publications

(1 citation statement)

References 60 publications

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“…The mechanism of ferroptosis in hepatocytes is thought to depend on the NF-κB signaling pathway. [85] Pg. infected hepatocytes exhibited heightened cell proliferation and migration, coupled with reduced doxorubicin-mediated apoptosis.…”

Section: Periodontal Problems and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Non-Alcoholic Fatty Liver and Periodontal Disease: Is there a Relationship? A Contemporary Review

Hatipoglu

2024

J Inonu Liver Transpl Inst

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T he Non-alcoholic fatty liver disease (NAFLD) it's a term used for several conditions caused by fat accumulation in the liver. One-fourth of the world's population is faced with this clinical situation. It is mostly seen in South America and the Middle East, and least in Africa. [1] Nevertheless, when considering its prevalence within the community, this malady emerges as one of the most frequently encountered liver diseases, demonstrating a notable association with elevated rates of liver-related mortality and morbidity. [2] By definition, NAFLD is a clinical picture in which insulin resistance, histopathological more than 5% steatosis of hepatocytes, or dense fat fractions by radiographic techniques are detected. This clinical situation is examined under two main headings non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (steatosis coexists with liver-cell injury and inflammation). [3,4] NAFLD has 4 stages for developing; simple fatty liver (steatosis), non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis, and may liver cancer. [5] In advanced phases, this may result in liver transplantation. The patients with NAFLD show similar histological damage to alcoholic liver disease. [6] Oxidative and inflammatory responses play crucial roles in the shared pathogenesis of both NAFLD and nonalcoholic NASH. [7] Lifestyle is an important point for developing this disease.Periodontal disease is a common inflammatory disease and is known to be related to other systemic diseases. This bidirectional relation between periodontal disease and other disease processes has led to outstanding research recently. In addition, periodontal disease has been advocated to exacerbate metabolic disorders including non-alcoholic fatty liver disease (NAFLD). In this traditional review, general characteristics of periodontal diseases, general characteristics of NAFLD/ Nonalcoholic steatohepatitis (NASH), and their causality were discussed for treatment providers. The collected data significantly corroborate a greater incidence of periodontal disease among individuals with NAFLD in comparison to the general healthy population. Healthcare professionals need to be aware of the association between NAFLD and periodontal disease thus patient management effectiveness can be enhanced.

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Section: Periodontal Problems and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Non-Alcoholic Fatty Liver and Periodontal Disease: Is there a Relationship? A Contemporary Review

Hatipoglu

2024

J Inonu Liver Transpl Inst

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Periodontal pathogen Fusobacterium nucleatum infection accelerates hepatic steatosis in high‐fat diet‐fed ApoE knockout mice by inhibiting Nrf2/Keap1 signaling

Wu,

Bie,

Zhou

et al. 2024

J of Periodontal Research

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AimsThis study sought to explore the impact of Fusobacterium nucleatum on hepatic steatosis in apolipoprotein E (ApoE) knockout (KO) mice induced by a high‐fat diet (HFD) and elucidate the underlying mechanism.MethodsApoE KO mice, on a HFD, received F. nucleatum oral inoculation every other day. After 24 weeks, body weight, liver weight, and liver index were assessed. Serum biochemistry and pro‐inflammatory factors in serum and liver were analyzed. The histopathology of right maxilla and live were performed. Oil red O, immunohistochemistry, and immunofluorescence staining for the liver were conducted. Myeloperoxidase (MPO) activity, apoptosis, lipid reactive oxygen species (ROS), ROS, lipid peroxides, and hepatic lipids were also evaluated. Liver inflammation, fibrosis, de novo lipogenesis (DNL)‐related molecule, and Nrf2/Keap1‐related signaling molecule gene/protein expression were determined by real‐time PCR (RT‐PCR) and/or Western blot (WB) analysis.ResultsHFD‐fed ApoE KO mice infected by F. nucleatum demonstrated significant changes, including increased body and liver weight, elevated proinflammatory factors and lipids in serum and liver, as well as neutrophil infiltration, fibrosis, apoptosis, oxidative stress, and lipid peroxidation in the liver. Additionally, F. nucleatum stimulates hepatic lipid accumulation and activates de novo lipogenesis (DNL), while simultaneously suppressing the Nrf2/Keap1 antioxidant pathway.ConclusionIn conclusion, our study reveals that oral inoculation of F. nucleatum might promote hepatic steatosis by inhibiting Nrf2/Keap1 pathway.

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Multifunctional role of oral bacteria in the progression of non-alcoholic fatty liver disease

Mei,

Yao,

Chen

et al. 2024

World J Hepatol

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Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver disorders of varying severity, ultimately leading to fibrosis. This spectrum primarily consists of NAFL and non-alcoholic steatohepatitis. The pathogenesis of NAFLD is closely associated with disturbances in the gut microbiota and impairment of the intestinal barrier. Non-gut commensal flora, particularly bacteria, play a pivotal role in the progression of NAFLD. Notably, Porphyromonas gingivalis , a principal bacterium involved in periodontitis, is known to facilitate lipid accumulation, augment immune responses, and induce insulin resistance, thereby exacerbating fibrosis in cases of periodontitis-associated NAFLD. The influence of oral microbiota on NAFLD via the “oral-gut-liver” axis is gaining recognition, offering a novel perspective for NAFLD management through microbial imbalance correction. This review endeavors to encapsulate the intricate roles of oral bacteria in NAFLD and explore underlying mechanisms, emphasizing microbial control strategies as a viable therapeutic avenue for NAFLD.

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Porphyromonas gingivalis triggers inflammation in hepatocyte depend on ferroptosis via activating the NF‐κB signaling pathway

Cited by 4 publications

References 60 publications

Non-Alcoholic Fatty Liver and Periodontal Disease: Is there a Relationship? A Contemporary Review

Non-Alcoholic Fatty Liver and Periodontal Disease: Is there a Relationship? A Contemporary Review

Periodontal pathogen Fusobacterium nucleatum infection accelerates hepatic steatosis in high‐fat diet‐fed ApoE knockout mice by inhibiting Nrf2/Keap1 signaling

Multifunctional role of oral bacteria in the progression of non-alcoholic fatty liver disease

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