Gnotobiotic and conventional mouse models of the IBD ATG16L1T300A SNP reveal gene-microbiota-immune interactions.

Overlapping action of type I, II, and III interferons maintains microbiome homeostasis, prevents IL-17-driven myeloproliferative disease, and protects against inflammatory bowel disease.

A multi-cohort analysis of 2,500 gut microbiomes and five major diseases discovers that disease-microbiome associations display specific age-centric trends, with diseases characterized by age-centric trends of species gain/loss.

The density of the gut microbiota influences the host immune system and adiposity, and can be therapeutically manipulated.

A novel multi-omics framework revealed the taxonomic contribution to microbiota oxalate, demontrated O. formigenes as the dominating taxon transcriptionally, and identified specific IBD cohort at risk for oxalte toxicity.

Experiments in a mouse model for Alzheimer’s disease using germ-free and conventionally housed animals reveal that microbiota-derived short-chain fatty acids promote the deposition of cerebral Aβ plaques.

Integration of clinical patient data, pathogen information and a multi-omic analysis of the gut microbiome reveals key determinants of disease in C. difficile-colonized patients.

A novel mathematical modeling framework for antibiotic-resistant bacteria combining within-host microbiome-pathogen interactions with population-level pathogen epidemiology, demonstrating how antibiotic consumption and ecological competition come together to drive the spread of resistance.

Bioinformatics analyses and experiments in mouse models reveal how Escherichia coli accesses the molecular hydrogen pool to boost colonization during acute colitis.

Microbial populations are continuous along the gastrointestinal tract, with increased transmission in colorectal cancer and rheumatoid arthritis patients.