Abstract
Increasing evidence indicates that chronic inflammation due to periodontal disease is associated with progression of non-alcoholic fatty liver disease (NAFLD) caused by a Western diet. NAFLD has also been associated with oral infection with the etiological agent of periodontal disease, Porphyromonas gingivalis. P. gingivalis oral infection has been shown to induce cardiometabolic disease features including hepatic lipid accumulation while also leading to dysbiosis of the gut microbiome. However, the impact of P. gingivalis infection on the gut microbiota of mice with diet-induced NAFLD and the potential for those changes to mediate NAFLD progression has yet to be determined. In the current study, we have demonstrated that P. gingivalis infection induced sustained alterations of the gut microbiota composition and predicted functions, which was associated with the promotion of NAFLD in steatotic mice. Reduced abundance of short-chain fatty acid-producing microbiota was observed after both acute and chronic P. gingivalis infection. Collectively, our findings demonstrate that P. gingivalis infection produces a persistent change in the gut microbiota composition and predicted functions that promotes steatosis and metabolic disease.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the most common liver condition in the Western world and increasingly necessitates liver transplantation [1, 2]
We demonstrate for the first time that the exacerbation of diet-induced steatosis and glucose intolerance by P. gingivalis oral infection of mice fed a Western diet (WD) is associated with distinct alterations in the gut microbiota composition and predicted functions, characterized by reductions in community diversity and short-chain fatty acid (SCFA) producers
To evaluate the influence of P. gingivalis infection on the progression of WD-induced NAFLD, steatosis and hepatic inflammation were evaluated by haematoxylin and eosin (H&E) staining of the liver (Figure 1A)
Summary
Non-alcoholic fatty liver disease (NAFLD) is the most common liver condition in the Western world and increasingly necessitates liver transplantation [1, 2]. NAFLD comprises a spectrum of progressive liver damage pathologies defined by hepatic lipid accumulation (steatosis). In over 40% of subjects with NAFLD, hepatic steatosis eventually progresses to non-alcoholic steatohepatitis (NASH), a state of hepatic inflammation which can eventually lead to advanced fibrosis, cirrhosis, and even liver cancer [3,4,5,6]. A disruption to the homeostasis of the complex gut microbiota, or gut dysbiosis, and microbial metabolite fluctuations are considered pathogenic factors in human NAFLD progression [8,9,10,11]. Lactate and short-chain fatty acids (SCFAs) are important metabolites produced by the gut microbiota and can directly promote host metabolism and suppress inflammation [12, 13]. Reduced production of Porphyromonas Exacerbates NAFLD and Dysbiosis certain SCFAs has been identified as an important pathogenic factor in NAFLD and some SCFA producers have been identified as potential therapeutic agents [14,15,16,17]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
