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Updated: Aug 16, 2025

Author Spotlight: Developing Immunocompetent Organ-on-Chip Models for Infectious Disease Research

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Published on: May 24, 2024

Capturing and Quantifying Particle Transcytosis with Microphysiological Intestine-on-Chip Models.

Ludivine C Delon^1,2, Matthew Faria³, Zhengyang Jia^1,2

¹Future Industries Institute, University of South Australia, Adelaide, SA, 5095, Australia.

|December 22, 2022

Summary

This summary is machine-generated.

Mechanical stimulation significantly enhances intestinal particle transport across Caco-2 cell monolayers. This intestine-on-chip model reveals a 350x higher transcytosis rate, crucial for drug delivery and environmental particle risk assessment.

Keywords:

cellular transcytosis enterocytes intestinal absorption intestine-on-chip

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Co-culture of Living Microbiome with Microengineered Human Intestinal Villi in a Gut-on-a-Chip Microfluidic Device

Published on: August 30, 2016

Area of Science:

Biomedical Engineering
Cell Biology
Pharmacology

Background:

Intestinal particle transport is vital for drug delivery and understanding environmental risks.
Caco-2 cell monolayers are standard models but lack polarized enterocyte transcytotic activity.

Purpose of the Study:

To investigate the effect of mechanical stimulation on intestinal particle transport using an intestine-on-chip model.
To compare particle transcytosis in static vs. fluid shear stress conditions.

Main Methods:

Utilized an intestine-on-chip microphysiological system combined with in silico modeling.
Exposed Caco-2 cell monolayers to fluid shear stress and compared to static cultures.
Analyzed transcytosis rates, energy dependence, and endocytic pathways (clathrin, macropinocytosis).

Main Results:

Fluid shear stress increased Caco-2 cell transcytosis by approximately 350x compared to static conditions.
Mechanical stimulation induced profound phenotypical alterations and a highly polarized cell state.
Transcytosis was energy-dependent, involving clathrin and macropinocytosis.
Increased transcytosis was attributed to enhanced internal particle transport (trafficking, exocytosis), not apical uptake.

Conclusions:

Mechanical stimulation via fluid shear stress dramatically enhances intestinal particle transcytosis in Caco-2 cells.
The intestine-on-chip model reveals key mechanisms of particle transport, including energy dependence and specific endocytic pathways.
Findings are critical for optimizing intestinal drug delivery and assessing risks from engineered and environmental particles.