Host–pathogen
Apical-out enteroids for pathogen access
Open access · cc by · source: Europe PMC
Suspending human enteroids without ECM flips polarity so microbes can meet the apical face.
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.
Human enteroids cultured in suspension without basement-membrane extract reversed polarity within hours; β1 integrin oriented that polarity so apical surfaces became accessible for pathogen assays. Confocal polarity markers are the readout; this is not a clinical infection trial, and enteroids only approximate gut immunity.
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.
Enteroid polarity reversed within hours without BME, with β1 integrin orienting apical pathogen access. Spike LYQD mutants altered S2 glycosylation mobility, and palmitoylation at cysteine clusters I/II was required for Golgi/plasma-membrane targeting and ACE2-mediated fusion. Those localisation phenotypes are IF/trafficking stains; enteroids are not a clinical gut, and much spike work uses pseudoviruses.
Evidence for the claim as stated.
IF is a screening camera in Vero cells (berzosertib 100 nM, 48 hpi), a tissue census in TB lung (35 patients), a trafficking assay for Smo/Rab5/spike, and a polarity assay in enteroids. 'Positive staining' in a drug screen is not the same claim as PD-1 on human tissue-resident T cells or as K140/K165 moving Rab5 off endosomes.
Evidence for the claim as stated.
Permeabilized-sperm SNARE timing and live epithelial polarity/spike trafficking disagree about how much native membrane regulation is still present. In-vitro sperm may miss in-vivo layers; enteroids and pseudovirus spike assays only approximate infection of a human airway or gut.
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 · How do proteins find plasmodesmata?
- Supports · How do gut-bacteria vesicles enter host cells?
- Supports · How do E. coli vesicles talk to gut epithelium?
IF is a screening camera in Vero cells (berzosertib 100 nM, 48 hpi), a tissue census in TB lung (35 patients), a trafficking assay for Smo/Rab5/spike, and a polarity assay in enteroids. 'Positive staining' in a drug screen is not the same claim as PD-1 on human tissue-resident T cells or as K140/K165 moving Rab5 off endosomes.
- Supports · ATR inhibitor blocks SARS-CoV-2
- Supports · PD-1 blockade reactivates TB via TNF
- Supports · How does monoubiquitin turn down Rab5?
Permeabilized-sperm SNARE timing and live epithelial polarity/spike trafficking disagree about how much native membrane regulation is still present. In-vitro sperm may miss in-vivo layers; enteroids and pseudovirus spike assays only approximate infection of a human airway or gut.
Study at a glance
- Design
- Animal / in-vitro — Human enteroids cultured in suspension without BME to reverse polarity for apical pathogen assays
- N
- Enteroid lines from multiple donors; assays often scored ~10 enteroids per well across experiments — no single primary N
- Population
- Human intestinal enteroids
- Outcome
- β1-integrin–dependent epithelial polarity orientation for host–pathogen assays
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
Apical-out enteroids for pathogen access
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
Human enteroids with controllable polarity.
Proper intestinal function depends on the development and maintenance of organization of epithelial cells into two distinct compartments, the apical and basolateral epithelial regions.
ECM / β1 integrin signaling.
The apical surface of intestinal epithelial cells (IECs) faces the lumen and regulates interactions with lumenal contents.
Key findings
Polarity reversed within hours; β1 integrin oriented polarity for apical pathogen assays.
Methodology
Human enteroids were cultured in suspension without BME; β1-integrin roles in polarity were tested.
Limitations
Not a clinical infection trial; enteroids only approximate gut immunity.
Related papers in this topic
Same topic cluster — not a recommendation engine.