colorectal-cancer

Fusobacterium nucleatum orchestrates immune suppression in colorectal cancer through multiple pathways.

Comprehensive review of Fusobacterium nucleatum (F. nucleatum) as an active co-conspirator in CRC rather than a passenger. F. nucleatum uses virulence factors (Fap2, FadA) for colonization and achieves immune evasion by inhibiting NK/T cells, recruiting MDSCs, driving Th17 polarization, suppressing CD8+ T cells, and upregulating PD-L1. May also enhance anti-PD-1/PD-L1 immunotherapy sensitivity. Therapeutic strategies include antibiotics, phages, virulence factor inhibitors, and combination immunotherapy.

Key Findings

F. nucleatum uses Fap2 and FadA for tumor colonization and immune evasion
Drives Th17 polarization while suppressing CD8+ T cell infiltration and promoting exhaustion
Upregulates PD-L1—potentially enhancing sensitivity to checkpoint immunotherapy
Collaborates with other microbes via quorum sensing and the oral-gut axis
F. nucleatum load serves as a non-invasive biomarker and prognosis predictor

Implications

F. nucleatum targeting offers therapeutic opportunities in CRC via antibiotics, phage therapy, or combination with immunotherapy. Its load may predict checkpoint inhibitor response.

Caveats

Review article; abstract-only. Most mechanistic evidence from preclinical models. Clinical translation of microbiome-targeting strategies remains challenging.

Source: Frontiers in immunology — 2026-01-01

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