ArticleNature materials2026
A transferable gut microbiota-bile acid pathway programs nanomedicine pharmacokinetics and therapeutic response.
Article in Nature materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Microbiota matter.Nature materials · 2026Article
- Host biology as a determinant of in vivo delivery and its translational potential.Clinical and translational medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors.
Funding
Abstract
The clinical efficacy of nanomedicines is often limited by hepatic sequestration, yet the endogenous programs determining this clearance state remain incompletely understood. Here we identify the gut microbiota as a regulator of nanomedicine biodistribution through bile-acid-associated programming of Kupffer cell phagocytic state. Using germ-free mice, microbial perturbation, faecal microbiota transplantation and multiomic profiling, we show that metronidazole remodels the gut microbial ecology and reprograms Kupffer cells into a reduced-uptake state, thereby suppressing hepatic clearance and enhancing the tumour accumulation of nanomedicines across multiple formulations and tumour models. Single-cell RNA sequencing reveals a shift in Kupffer cell populations from phagocytic to quiescent states, whereas metabolomic profiling identifies microbiota-dependent reductions in bile acid availability. Gut-bacteria-derived bile acids induce Kupffer cell phagocytosis, and faecal transfer transmits the low-clearance phenotype, defining a transferable gut microbiota-bile acid-Kupffer cell pathway affecting nanomedicine clearance.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.