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In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
Published on: October 19, 2018
IL-1beta causes an increase in intestinal epithelial tight junction permeability
1Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|March 21, 2007
Summary
Interleukin-1 beta (IL-1beta) increases intestinal epithelial permeability by activating NF-kappaB pathways. This study clarifies IL-1beta
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Proinflammatory cytokines like IL-1beta are key in intestinal inflammation.
- TNF-alpha and IFN-gamma increase intestinal permeability, but IL-1beta's role is unclear.
Purpose of the Study:
- To investigate IL-1beta's effect on intestinal epithelial tight junction (TJ) barrier function.
- To elucidate the mechanisms underlying IL-1beta's impact on TJ permeability.
Main Methods:
- Utilized an in vitro model of Caco-2 intestinal epithelial monolayers.
- Measured transepithelial electrical resistance and paracellular permeability to inulin.
- Assessed NF-kappaB activation, inhibition, and p65 silencing via siRNA.
- Evaluated IL-1beta's effect on Caco-2 cell apoptosis.
Main Results:
- IL-1beta decreased Caco-2 transepithelial resistance and increased inulin permeability in a dose- and time-dependent manner.
- IL-1beta rapidly activated NF-kappaB, which was inhibited by NF-kappaB inhibitors and siRNA depletion of p65.
- IL-1beta did not induce apoptosis in Caco-2 cells.
Conclusions:
- IL-1beta increases intestinal epithelial TJ permeability at physiologically relevant concentrations.
- This increase is mediated, in part, by NF-kappaB pathway activation.
- Apoptosis is not the mechanism behind IL-1beta-induced TJ permeability changes.
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