Microbiome
How do gut-bacteria vesicles enter host cells?
Open access · cc by · source: Europe PMC
B. thetaiotaomicron outer-membrane vesicles are taken up within minutes via dynamin-dependent endocytosis/macropinocytosis and traffic to Golgi/ER/lysosomes.
Study at a glance
- Design
- Animal / in-vitro — Live imaging of B. thetaiotaomicron OMVs on intestinal epithelial cells/organoids
- N
- Cell/organoid trafficking assays — no single primary analytic N in stored text
- Population
- Intestinal epithelial cells and organoids exposed to Bt OMVs
- Outcome
- Uptake routes and intracellular biodistribution of bacterial OMVs
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Uptake within ~15 min; mainly dynamin-dependent endocytosis or macropinocytosis; vesicles reach Golgi/ER/nucleus routes and accumulate in lysosomes.
Methodology
Live imaging and trafficking assays of Bt OMVs on intestinal epithelial cells/organoids, with endocytosis inhibitors and organelle markers.
Limitations
Does not prove every in vivo systemic effect of OMVs in humans.
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.
Bacteroides thetaiotaomicron outer-membrane vesicles were taken up by intestinal epithelial cells and organoids within about 15 minutes, mainly by dynamin-dependent endocytosis or macropinocytosis, then reached Golgi/ER/nucleus routes and accumulated in lysosomes. Live imaging plus organelle markers and endocytosis inhibitors supplied that itinerary; systemic human effects are not proven.
Evidence for the claim as stated.
Confocal is used here for polarity reversal (enteroids), plasmodesmal targeting (PDLP), and vesicle itineraries (Bt OMVs in ~15 min; E. coli OMVs to NOD sensors). Those are different spatial questions — which face of an epithelium, which plant cell-wall channel, which endocytic route — and cannot be pooled as one 'trafficking phenotype'.
Evidence for the claim as stated.
Bacteroides thetaiotaomicron OMVs entered epithelial cells and organoids within about 15 minutes via dynamin-dependent endocytosis or macropinocytosis, then reached Golgi/ER/nucleus routes and lysosomes. That itinerary is live imaging with inhibitors and organelle markers — confocal-scale trafficking — not a proof of every systemic human effect, and not primarily transmission-EM reconstruction.
Evidence for the claim as stated.
Only the caveolar paper is clearly an ultrastructure-of-a-coat study. GPCR work compares 142 inactive and 27 active deposited structures; APEX2 is proteomics; salmon work is a 30-day transcriptome of fat-cell differentiation; Bt OMV uptake is live light-microscopy trafficking. Calling all five 'electron microscopy papers' overstates shared methods.
Evidence for the claim as stated.
Resolution targets disagree. Caveolar EM asks about coat stoichiometry (Cavin 1 trimers; exclusion of EHD2/pacsin 2). GPCR contact maps ask about conserved switches across receptors (34 residue pairs). OMV live imaging asks about a 15-minute endocytic route. Those answers cannot substitute for one another.
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.
Confocal is used here for polarity reversal (enteroids), plasmodesmal targeting (PDLP), and vesicle itineraries (Bt OMVs in ~15 min; E. coli OMVs to NOD sensors). Those are different spatial questions — which face of an epithelium, which plant cell-wall channel, which endocytic route — and cannot be pooled as one 'trafficking phenotype'.
- Supports · Apical-out enteroids for pathogen access
- Supports · How do proteins find plasmodesmata?
- Supports · How do E. coli vesicles talk to gut epithelium?
Only the caveolar paper is clearly an ultrastructure-of-a-coat study. GPCR work compares 142 inactive and 27 active deposited structures; APEX2 is proteomics; salmon work is a 30-day transcriptome of fat-cell differentiation; Bt OMV uptake is live light-microscopy trafficking. Calling all five 'electron microscopy papers' overstates shared methods.
- Supports · What proteins build the caveolar coat?
- Supports · Shared class A GPCR activation path
- Supports · Mapping the faces of mitochondria and ER
- Supports · Salmon fat-cell differentiation transcriptome
Resolution targets disagree. Caveolar EM asks about coat stoichiometry (Cavin 1 trimers; exclusion of EHD2/pacsin 2). GPCR contact maps ask about conserved switches across receptors (34 residue pairs). OMV live imaging asks about a 15-minute endocytic route. Those answers cannot substitute for one another.
- Supports · What proteins build the caveolar coat?
- Supports · Shared class A GPCR activation path
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