ArticleMicrobiome2026
Metabolic host-microbe crosstalk in stabilization of epithelial HIF.
Article in Microbiome, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
backgroundThe gastrointestinal tract is home to trillions of microorganisms that interact with their host in profound ways. One mechanism by which these microbes interact with their eukaryotic host is through the establishment of "physiologic hypoxia" in the intestinal mucosa, which has been shown to promote gut barrier function and homeostasis in a hypoxia-inducible factor (HIF)-dependent manner. The association between HIF and intestinal homeostasis has been long understood, as activation of HIF signaling has been shown to promote barrier function both in vitro and in vivo. Although it has been previously established that pathogenic bacteria regulate HIF stabilization and activity in the intestinal epithelium independent of short-chain fatty acid metabolism, it is not clear whether this activity extends to noninfectious and/or commensal bacterial species.
resultsHere, we demonstrate that nonpathogenic, commensal strains of Escherichia coli stabilize HIF in intestinal epithelial cells in vitro. Further, we show that HIF is transcriptionally active in epithelia and drives a "pro-barrier" transcriptional program. This property was found to be dependent on bacterial aerobic respiration, as genetic elimination of E. coli aerobic respiration abolished HIF stabilization and the subsequent transcriptional phenotype. Finally, we observed stabilization of tissue HIF-1α in vivo using antibiotic-treated mice colonized with wild-type, but not respiration-deficient, E. coli.
conclusionsThese findings demonstrate a novel ability for commensal E. coli to regulate intestinal homeostasis through activation of HIF and suggest that this mechanism might be a major component of the interaction between facultative anaerobes and the intestinal epithelium in the gut. In addition, we hypothesize that consumption of oxygen by enteric bacteria might be leveraged as a novel therapeutic to combat intestinal inflammation, such as that observed during inflammatory bowel disease (IBD). Video Abstract.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.