Figure 2.

Upper section: Fusobacterium nucleatum (Fn) is involved in the formation of the subgingival biofilm by aggregating with primary and secondary colonisers and other species such as Candida albicans. through adhesin RasD. It leads the subgingival biofilm towards a dysbiosis state through AI2. The inflammatory process at the gingival level progresses to periodontitis and alveolar bone destruction. Middle section: Fn, through its adhesion molecule FadA, binds to E-cadherin in the endothelial cells of the gingival blood vessels, altering the permeability of these vessels and passing into the bloodstream (indirect diffusion). Pro-inflammatory cytokines from the gingival inflammatory process also pass into the bloodstream. Lower section: Fn in the intestinal lumen through LPS and FadA, activating TLR-4 and β-catenin, induces the synthesis of oncogenes by enterocytes, causing a dysbiosis of the colonic microbiome. In an already developed tumour, it would bind to Gal/GalNAc expressed on the tumour cell surface and evade the anti-tumour immune action of NK-Cell and lymphocytes. Fn can also bind to the metastatic tumour cell and, therefore, travel to other organs such as the liver (star in the graph).