Which pathway is suggested to link Fusobacterium to NF-κB activation in the gut?

• A. TLR2/MyD88
• B. NOD-like receptor pathway
• C. RIG-I/MAVS
• D. TLR4/MYD88

Answer: (D)

Fusobacterium in the gut is most commonly linked to NF-κB activation through the TLR4-MYD88 signaling axis. The bacterium’s outer surface components, notably LPS, are recognized by Toll-like receptor 4 on intestinal epithelial and immune cells. This recognition recruits the adaptor protein MyD88, triggering a cascade that activates the IKK complex, leads to degradation of IκB, and allows NF-κB to move into the nucleus. There NF-κB promotes transcription of pro-inflammatory cytokines and chemokines, driving inflammatory responses in the gut.

While other pathways exist for activating NF-κB, such as NOD-like receptors sensing intracellular peptidoglycan or RIG-I/MAVS sensing RNA, and TLR2 pathways, the link between Fusobacterium and gut NF-κB activation is most consistently explained by the TLR4/MyD88 route because of the bacterial LPS-TLR4 interaction. This makes it the best-fitting mechanism for the described association.