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Updated: May 6, 2026

In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
Published on: October 19, 2018
Changes in intestinal permeability and epithelial differentiation during inflammation in the rat
J K Ramage1, R H Hunt, M H Perdue
1Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Nippostrongylus brasiliensis infection increases gut permeability in rats, particularly in the jejunum, during early and acute stages. This change is localized, reversible, and linked to undifferentiated epithelial cells.
Area of Science:
- Gastroenterology
- Parasitology
- Immunology
Background:
- Gut permeability is crucial for intestinal health.
- Inflammation can disrupt the intestinal barrier.
- Nippostrongylus brasiliensis is a nematode parasite that induces an inflammatory response in rats.
Purpose of the Study:
- To investigate changes in gut permeability during Nippostrongylus brasiliensis infection in a rat model.
- To determine the localization and reversibility of altered gut permeability.
- To correlate permeability changes with intestinal morphological alterations.
Main Methods:
- Rats were infected with Nippostrongylus brasiliensis.
- Gut permeability was assessed using 51Cr-EDTA as a probe in ligated jejunal loops.
- Radioactivity was measured in urine, kidney, and the intestinal loop.
- Intestinal morphology (villus atrophy, crypt hyperplasia) was examined.
Main Results:
- Urinary recovery of 51Cr-EDTA significantly increased during early (day 7) and acute (day 10) infection stages.
- Increased permeability was localized to the inflamed jejunum; the terminal ileum remained normal.
- Villus atrophy and crypt hyperplasia were observed during infection.
- Permeability returned to normal as the infection resolved.
Conclusions:
- Nippostrongylus brasiliensis infection causes transient, localized increases in gut permeability in the jejunum.
- The observed permeability changes are reversible upon parasite clearance.
- Altered gut permeability may be associated with an increased proportion of undifferentiated epithelial cells at the site of inflammation.
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