![]() T helper 17 cells (Th17) are a subset of T cells that mainly secrete proinflammatory factors such as IL-17 and IL-22 and differentiate from naïve T cells under the stimulation of IL-6 and TGF-β. However, the underlying mechanisms that overlap between the conditions remain unclear. In fact, both diseases are characterized by an excessive and nonself-limiting immune response to the dysbiotic microbiome 10. There is substantial evidence for the association between IBD and periodontitis 8, 9. IBD is a specific type of intestinal inflammation and is classified into two major forms, Crohn’s disease (CD) and ulcerative colitis (UC). ![]() The intrinsic mechanisms involve distant spread and ectopic infection by periodontopathogens, distal end migration of oral inflammatory-activated Th17 cells, and metabolic and immune disorders 7. Periodontitis has a major impact on various systemic diseases, including inflammatory bowel disease (IBD) 3, 4, 5, Type 2 diabetes mellitus (T2D), metabolic syndrome, and coronary heart disease 6. Among them, the gram-negative anaerobic microbe Porphyromonas gingivalis (Pg) functions as a keystone pathogen and possesses an array of virulence factors 2. Periodontitis patients may swallow 10 1~10 13 bacteria in saliva every day 1. Periodontitis is an inflammatory response triggered by pathogenic microorganisms in the oral cavity and is the leading cause of tooth loss in humans. Our study suggests that Pg aggravates colitis via a gut microbiota-LA metabolism-Th17/Treg cell balance axis, providing a potential therapeutically modifiable target for IBD patients with periodontitis. Therapeutically restoring LA levels in colitis mice challenged with Pg exerts anti-colitis effects by decreasing the Th17/Treg cell ratio in an AHR-dependent manner. ![]() Nevertheless, it suppresses the linoleic acid (LA) pathway in the gut microbiota, which was the target metabolite that determines the degree of inflammation and functions as an aryl hydrocarbon receptor (AHR) ligand to suppress Th17 differentiation while promoting Treg cell differentiation via the phosphorylation of Stat1 at Ser727. Specifically, metagenomic and metabolomic analyses shows that oral administration of Pg increases levels of the Bacteroides phylum but decreases levels of the Firmicutes, Verrucomicrobia, and Actinobacteria phyla. We demonstrate that the critical periodontal pathogen Porphyromonas gingivalis (Pg) aggravates intestinal inflammation and Th17/Treg cell imbalance in a gut microbiota-dependent manner. ![]() However, the underlying mechanisms that overlap still need to be clarified. An excessive and non-self-limiting immune response to the dysbiotic microbiome characterizes the two. Periodontitis is closely related to inflammatory bowel disease (IBD). ![]()
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