A bottom-up designed seven-species synthetic microbial community for ecological control of Fusobacterium nucleatum-associated colorectal cancer models.
Taxonomy
| Taxon | Ontology ID | Functional Roles | Abundance |
|---|---|---|---|
| seven commensal bacterial SynCom members — ontology label: Bacteria | NCBITaxon:2 · TaxonMech · TraitMech |
CROSS_FEEDER
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N/A |
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Ecological Interactions
The graph shows only explicitly linked interaction participants. Community members without an asserted participant link are omitted; membership alone does not imply an interaction.
Low-Competition Commensal SynCom Colonization
A seven-species SynCom selected using metabolic-network criteria was tested for colonization in an AOM-DSS mouse CRC model. Low modeled competition is a design criterion, not demonstrated niche partitioning or isolated evidence that colonization causes F. nucleatum suppression. F. nucleatum and SynCom were mixed before gavage in the combination arm.
Biological Processes:
- biological process involved in interspecies interaction between organisms (GO:0044419 · PathwayMech)
Evidence
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PMID:40433987 - SUPPORT (IN_VIVO)"A synthetic microbial community (SynCom) is then designed by metabolic network reconstruction, and its performance is validated using coculture experiments and an AOM-DSS induced mouse CRC model."
Fusobacterium nucleatum Ecological Suppression
The SynCom inhibited F. nucleatum in vitro and lowered its abundance in the mouse experiment. The paper classifies many pair interactions as exploitation, not reciprocal-negative competition under this schema. Amino-acid supplementation reduced acidity and slowed F. nucleatum decline, supporting context-dependent inhibition rather than tryptophan-enhanced suppression. Co-gavage does not cleanly establish eradication of a previously established infection.
Metabolites: L-tryptophan (CHEBI:16828 · MediaIngredientMech · CMMMech)
Evidence
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PMID:40433987 - SUPPORT (IN_VIVO)"A synthetic microbial community (SynCom) is then designed by metabolic network reconstruction, and its performance is validated using coculture experiments and an AOM-DSS induced mouse CRC model."
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PMID:40433987 - SUPPORT (IN_VIVO)"it promotes F. nucleatum decolonization, and enhances tryptophan metabolism and secondary bile acid conversion"
Tryptophan and Secondary Bile Acid Restoration
SynCom treatment was associated with altered tryptophan metabolism and secondary bile-acid profiles in the mouse model. PARTIAL - the authors propose that these changes contribute to disease outcomes, but metabolite correlations and expression do not establish necessary mediation. The main-text versus figure definitions of the LCA conversion ratio differ, so no numerical conversion direction is inferred here.
Metabolites: L-tryptophan (CHEBI:16828 · MediaIngredientMech · CMMMech), bile acid (CHEBI:3098 · MediaIngredientMech · CMMMech)
PARTIAL - altered tryptophan and bile-acid metabolism could contribute to reduced tissue lipid accumulation, inflammation and tumor burden, as proposed by the source. The experiments do not isolate these metabolites as necessary mediators of SynCom benefit or establish clinical efficacy.
Evidence
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PMID:40433987 - PARTIAL (IN_VIVO)"enhances tryptophan metabolism and secondary bile acid conversion, leading to reduced lipid accumulation, decreased inflammatory reaction, and enhanced tumor inhibition effect"
Reduced Inflammation and Tumor Burden
The SynCom combination arm reduced measured tumor and inflammatory endpoints and tissue lipid accumulation in the F. nucleatum-treated AOM-DSS mouse model. Blood triglyceride reduction was nonsignificant. There was no disease-model SynCom-only arm without F. nucleatum, and these results do not establish efficacy in human colorectal cancer.
Biological Processes:
- biological process involved in interspecies interaction between organisms (GO:0044419 · PathwayMech)
Evidence
-
PMID:40433987 - SUPPORT (IN_VIVO)"leading to reduced lipid accumulation, decreased inflammatory reaction, and enhanced tumor inhibition effect"
Knowledge gaps & discussions (1)
KNOWLEDGE_GAP OPEN Do separated colonization, infection and metabolite interventions establish the proposed causal chain?
Remove colonization-to-suppression and suppression-to-metabolism arrows: design and concurrent intervention outcomes do not isolate those mechanisms. Retain metabolism-to-disease only as PARTIAL source interpretation. Co-gavage, missing SynCom-only disease-model arm, inconsistent pH correlation wording and LCA ratio definitions limit attribution; model feature importance is not causal mediation. Full main text/captions read, not images or supplements. Seven-species roster recovery remains #1268; obsolete GO:0006568 stays absent (#1213).
Attaches to: ecological_interactions#Low-Competition Commensal SynCom Colonization, ecological_interactions#Fusobacterium nucleatum Ecological Suppression, ecological_interactions#Tryptophan and Secondary Bile Acid Restoration, ecological_interactions#Reduced Inflammation and Tumor Burden
Environmental Factors
| Factor | Value | Unit |
|---|---|---|
| metabolic network reconstruction design | A seven-species SynCom with low competitive interrelationships was designed from human metagenome and metabolomics data. | N/A |
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Growth Media
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