Figure 3.

Known pathways induced by F. nucleatum binding that result in increased interleukin-8 (IL-8) secretion. (a) F. nucleatum infection in Caco-2 colorectal cancer cells impaired autophagic flux, which enhanced the production of TNF-α, IL-1β and IL-8 via the increase in reactive oxygen species (ROS). (b) F. nucleatum binding via its FadA adhesin to the sugar D-galactose-β(1–3)-N-acetyl-D-galactosamine (Gal-GalNAc) on colorectal cancer cells enables invasion, which further stimulates the release of IL-8 and CXCL1. (c) Outer membrane vesicles and the porin FomA secreted by F. nucleatum stimulate Toll-like receptors (TLRs) 2 and 4 on colonic epithelial cells, inducing NF-κB signalling that results in increased IL-8 secretion. (d) F. nucleatum's FadA adhesin binds to E-cadherin, activating β-catenin signalling in CRC cells, resulting in increased expression of pro-inflammatory cytokines, including IL-8. Figure created with BioRender.