NFKB1 and inflammatory bowel disease: Internalized GBEVs further trigger the formation of NOD1 aggregates in IECs, which activates the NF-κB signaling pathway and promotes the expression of inflammatory factors IL-6 and IL-8 (Figure 4A).88 While the sustained stimulation of NOD1 by GBEVs from both sources results in an inflammatory response, GBEVs secreted by E. coli Nissle 1917 and Commensal ECOR63 promote the expression of tight junction proteins in IECs, thereby improving IBD.103 Therefore, the biological effects of GBEVs should be evaluated from multiple perspectives, and should not be judged by a single indicator.