Bidirectional regulation of the gut microbiome-immune axis in the immune microenvironment of colorectal cancer and targeted interventions

Table 1 Comparative impact of gut microbiota interventions on immune regulation and colorectal cancer therapy outcomes

Intervention	Key microbes	Mechanism of action	Impact on CRC treatment
Prognostic Biomarker	Fn/Fp ratio	Fn promotes inflammation and tumorigenesis, while Fp has anti-inflammatory and protective effects; Fn/Fp ratio reflects tumor microenvironment status	Higher Fn abundance correlates with poor prognosis, while higher Fp levels associate with better outcomes; Fn/Fp ratio aids in early screening and prognosis assessment
Enhance Chemosensitivity	NaB-producing bacteria (e.g., Faecalibacterium) and NaB	NaB strengthens gut barrier function, modulates immune activity, and induces tumor cell apoptosis while inhibiting proliferation, migration, and invasion	Improves efficacy of OXA and other chemotherapies while reducing side effects
Modulate Immunotherapy Response	B. fragilis (polysaccharides), Fn (succinic acid)	(1) B. fragilis polysaccharides synergize with CTLA-4 inhibitors to activate T cells; and (2) Fn-derived succinate inhibits the cGAS-interferon-β pathway, reducing CD8+ Tcells infiltration	(1) Enhances immune checkpoint inhibitor efficacy; and (2) High Fn abundance causes anti-PD-1 resistance, reversible via antibiotics or microbiota modulation

CRC: Colorectal cancer; Fn: Fusobacterium nucleatum; Fp: Faecalibacterium; OXA: Oxaliplatin; NaB: Butyrate; CD: Cluster of differentiation; CTLA-4: Cytotoxic T-lymphocyte-associated protein 4; cGAS Cyclic: GMP-AMP synthase; PD-1: Programmed cell death protein 1; B. fragilis: Bacteroides fragilis.