Microbiome
Infant diet shapes gut–host immunity
Open access · cc by · source: Europe PMC
Breast- vs formula-fed infants differ in gut microbiota and host immune gene expression.
Study at a glance
- Design
- Cross-sectional — Infant stool metagenomes correlated with host epithelial transcriptomes by feeding mode
- N
- N=12 · Six breast-fed and six formula-fed infants
- Population
- Breast-fed and formula-fed human infants
- Outcome
- Diet-linked microbiota composition and host intestinal/immunity gene expression
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Diet altered Firmicutes/Actinobacteria composition; 459 intestinal and 660 immunity genes were tested, with many differentially expressed between diets.
Methodology
Sequenced stool metagenomes and profiled host epithelial mRNA from 6 breast-fed and 6 formula-fed infants, then correlated taxa/genes with host transcripts.
Limitations
Small n; association does not prove which microbes cause each transcript change.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
16S-style community profiles are sometimes paired with metabolites or, in infants, with shotgun metagenomes and host transcripts. A METSIM subset linked gut microbes to plasma metabolites and metabolic traits in Finnish men; six breast-fed versus six formula-fed infants showed diet-altered Firmicutes/Actinobacteria and many differentially expressed host immunity genes.
Evidence for the claim as stated.
Marker-gene 16S and shotgun metagenomes answer different questions in this set. HMP biogeography and the bee pesticide paper are amplicon community maps (the bee paper adds ITS); the infant diet paper sequences stool metagenomes and host mRNA. Treating every 'microbiome sequencing' paper as 16S genus tables hides the extra functional genes the infant paper actually uses.
Evidence for the claim as stated.
Stool metagenomes plus epithelial mRNA from 6 breast-fed and 6 formula-fed infants showed diet-altered Firmicutes/Actinobacteria composition. The study tested 459 intestinal and 660 immunity genes, with many differentially expressed between diets. Small n and correlation do not prove which microbes cause each transcript change.
Evidence for the claim as stated.
Shotgun gene-content metagenomics (within-species deletions across people; infant diet genes plus 459/660 host transcripts; B. dorei before seroconversion) is not the same experiment as HMP-style 16S biogeography (>24 million reads, 2,983 specimens, ~8,167 V3–V5 reads). A 16S habitat map cannot report accessory genes; a gene-deletion call cannot replace body-wide taxonomy.
Evidence for the claim as stated.
Even among shotgun studies, claims differ in strength. Infant diet work is n=6 versus 6 with host-transcript correlations; DIPP is 76 children and 947 samples but still does not prove B. dorei causes autoimmunity; within-species gene content varies without assigning a disease. Pooling them as 'the microbiome causes immunity' overreads every design.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Marker-gene 16S and shotgun metagenomes answer different questions in this set. HMP biogeography and the bee pesticide paper are amplicon community maps (the bee paper adds ITS); the infant diet paper sequences stool metagenomes and host mRNA. Treating every 'microbiome sequencing' paper as 16S genus tables hides the extra functional genes the infant paper actually uses.
- Supports · Human body microbiome biogeography
- Supports · Pesticides reshape honey bee gut microbes
Shotgun gene-content metagenomics (within-species deletions across people; infant diet genes plus 459/660 host transcripts; B. dorei before seroconversion) is not the same experiment as HMP-style 16S biogeography (>24 million reads, 2,983 specimens, ~8,167 V3–V5 reads). A 16S habitat map cannot report accessory genes; a gene-deletion call cannot replace body-wide taxonomy.
- Supports · How much do gut bacterial gene contents differ?
- Supports · B. dorei rises before T1D autoimmunity
- Supports · Human body microbiome biogeography
Even among shotgun studies, claims differ in strength. Infant diet work is n=6 versus 6 with host-transcript correlations; DIPP is 76 children and 947 samples but still does not prove B. dorei causes autoimmunity; within-species gene content varies without assigning a disease. Pooling them as 'the microbiome causes immunity' overreads every design.
- Supports · B. dorei rises before T1D autoimmunity
- Supports · How much do gut bacterial gene contents differ?
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