Apical-out enteroids for pathogen access
Suspending human enteroids without ECM flips polarity so microbes can meet the apical face.
Source
Controlling Epithelial Polarity: A Human Enteroid Model for Host-Pathogen Interactions
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
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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.
What they did
Human enteroids were cultured in suspension without BME; β1-integrin roles in polarity were tested.
What they found
Polarity reversed within hours; β1 integrin oriented polarity for apical pathogen assays.
The limits
What it doesn't show
Not a clinical infection trial; enteroids only approximate gut immunity.
Key terms
- Enteroid
- 3D intestinal stem-cell culture.
- Apical-out
- Apical membrane faces medium.
- β1 integrin
- ECM receptor steering polarity.
- BME
- Basement-membrane extract scaffold.
- Polarity
- Apical vs basolateral organization.
- Host–pathogen
- Microbe–epithelium interaction.
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Topic:
Common questions
How reverse?
Suspension without ECM.
Key receptor?
β1 integrin.
Why useful?
Apical microbe access.
Species?
Human.
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