Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role of Porphyromonas gingivalis

Abstract

Gut microbiota play many important roles, such as the regulation of immunity and barrier function in the intestine, and are crucial for maintaining homeostasis in living organisms. The disruption in microbiota is called dysbiosis, which has been associated with various chronic inflammatory conditions, food allergies, colorectal cancer, etc. The gut microbiota is also affected by several other factors such as diet, antibiotics and other medications, or bacterial and viral infections. Moreover, there are some reports on the oral-gut-liver axis indicating that the disruption of oral microbiota affects the intestinal biota. Non-alcoholic fatty liver disease (NAFLD) is one of the systemic diseases caused due to the dysregulation of the oral-gut-liver axis. NAFLD is the most common liver disease reported in the developed countries. It includes liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer. Recently, accumulating evidence supports an association between NAFLD and dysbiosis of oral and gut microbiota. Periodontopathic bacteria, especially Porphyromonas gingivalis, have been correlated with the pathogenesis and development of NAFLD based on the clinical and basic research, and immunology. P. gingivalis was detected in the liver, and lipopolysaccharide from this bacteria has been shown to be involved in the progression of NAFLD, thereby indicating a direct role of P. gingivalis in NAFLD. Moreover, P. gingivalis induces dysbiosis of gut microbiota, which promotes the progression of NAFLD, through disrupting both metabolic and immunologic pathways. Here, we review the roles of microbial dysbiosis in NAFLD. Focusing on P. gingivalis, we evaluate and summarize the most recent advances in our understanding of the relationship between oral-gut microbiome symbiosis and the pathogenesis and progression of non-alcoholic fatty liver disease, as well as discuss novel strategies targeting both P. gingivalis and microbial dysbiosis.

Comparison of the Oral Microbiota Structure among People from the Same Ethnic Group Living in Different Environments

“…We hypothesize that when the balance of the oral microbial community structure is disturbed, this may lead to the development of oral diseases [ 62 ]. Prevotella , Porphyromonas , and Leptotrichia are known as pathogens that cause oral disease [ 63 – 65 ]. In the UH group, Prevotella melaninogenica , Leptotrichia wadei , and Porphyromonas pasteri were closely linked with other flora, which supports our hypothesis.…”

Exploration of Shared Gene Signatures and Molecular Mechanisms Between Periodontitis and Nonalcoholic Fatty Liver Disease

“…Second, metabolite of intestinal bacteria results in fatty degeneration of liver cells, insulin resistance, and hepatic fibrosis ( Ji et al, 2019 ). Third, endotoxemia attributed to the increase in intestinal permeability is related to pathogenesis of NAFLD ( Wang et al, 2022 ). However, the mechanism of the pathology in which the intestinal flora imbalance induced by oral bacteria contributes to NAFLD has been unclear.…”

“…However, the mechanism of the pathology in which the intestinal flora imbalance induced by oral bacteria contributes to NAFLD has been unclear. Studies have pointed out that Porphyromonas gingivalis plays a major role in the process via interfering with the metabolic and immune profiles ( Wang et al, 2022 ). It is not clear if DCs also affect the transmission of pathogenic bacteria and their toxic metabolites to the liver through the portal vein.…”

Porphyromonas gingivalis: A key role in Parkinson's disease with cognitive impairment?

“…Animal studies showed that the oral administration of P. gingivalis at simulated doses causes gut microbiota dysbiosis and gut permeability impairment, resulting in systemic inflammation in mice ( 80 , 81 ). It was reported that P. gingivalis -induced dysbiosis is related to arthritis ( 65 , 82 ), type 2 diabetes ( 83 ), and non-alcoholic fatty liver disease (NAFLD) ( 84 ).…”