The bidirectional biological interplay between microbiome and viruses in periodontitis and type-2 diabetes mellitus.

Periodontitis was an inflammatory disease associated with a dysbiosis of the oral flora characterized by a chronic sustained inflammation inducing the resorption of alveolar bone and leading to tooth loss. Type 2 diabetes mellitus (T2D) was a metabolic disease caused by impaired insulin action. The oral microbiome played a crucial role in modulating both the innate and adaptive immune system during the trigger and exacerbation of periodontitis and T2D. The bidirectional relationship of T2D and periodontitis had been the focus of intensive research, but those were not well explored. In this commentary, an in-depth analysis of the changes of microbiome and bacterial metabolites in periodontitis with or without diabetes was described. The promotion of periodontitis to T2D might involve inflammatory factors/receptors, oxidative stress, microRNA and so on. The effect of diabetes on periodontitis might involve adipose factor pathway, AGE/RAGE and RANK/RANKL pathway etc. Generally, periodontitis and diabetes are closely related to the microecological-epithelial interaction, soft tissue degradation, bone coupling disorder, immune regulation and gene transcription. The viruses, including HBV, HCV, HSV-1, Coronavirus, HCMV, EBV, HIV, phageome and so on, played an important role in the development of T2D and periodontitis. An in-depth understanding of the relationship between microbiome and host was of great significance to clarify the bidirectional mechanisms, suggesting that the periodontitis or T2D remission will have a positive impact on the other.

Microbiota regulation of viral infections through interferon signaling.

The interferon (IFN) response is the major early innate immune response against invading viral pathogens and is even capable of mediating sterilizing antiviral immunity without the support of the adaptive immune system. Cumulative evidence suggests that the gut microbiota can modulate IFN responses, indirectly determining virological outcomes. This review outlines our current knowledge of the interactions between the gut microbiota and IFN responses and dissects the different mechanisms by which the gut microbiota may alter IFN expression to diverse viral infections. This knowledge offers a basis for translating experimental evidence from animal studies into the human context and identifies avenues for leveraging the gut microbiota-IFN-virus axis to improve control of viral infections and performance of viral vaccines.

Gut microbiota and renin-angiotensin system: a complex interplay at local and systemic levels.

Gut microbiota is a potent biological modulator of many physiological and pathological states. The renin-angiotensin system (RAS), including the local gastrointestinal RAS (GI RAS), emerges as a potential mediator of microbiota-related effects. The RAS is involved in cardiovascular system homeostasis, water-electrolyte balance, intestinal absorption, glycemic control, inflammation, carcinogenesis, and aging-related processes. Ample evidence suggests a bidirectional interaction between the microbiome and RAS. On the one hand, gut bacteria and their metabolites may modulate GI and systemic RAS. On the other hand, changes in the intestinal habitat caused by alterations in RAS may shape microbiota metabolic activity and composition. Notably, the pharmacodynamic effects of the RAS-targeted therapies may be in part mediated by the intestinal RAS and changes in the microbiome. This review summarizes studies on gut microbiota and RAS physiology. Expanding the research on this topic may lay the foundation for new therapeutic paradigms in gastrointestinal diseases and multiple systemic disorders.