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Apoptosis and intestinal barrier function
C Bojarski1, K Bendfeldt, A H Gitter
1Department of Gastroenterology, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, 12200 Berlin, Germany.
Annals of the New York Academy of Sciences
|February 24, 2001
Summary
Camptothecin induces apoptosis in intestinal cells, significantly weakening the epithelial barrier. This study reveals how apoptosis impacts intestinal barrier function, paving the way for further research.
Area of Science:
- Gastrointestinal physiology
- Cell biology
- Molecular signaling
Background:
- Apoptosis induction pathways in the gastrointestinal tract are partially understood.
- The impact of apoptotic signals on intestinal barrier function remains largely unknown.
Purpose of the Study:
- To investigate the effect of camptothecin-induced apoptosis on HT-29/B6 intestinal cell monolayers.
- To characterize the influence of apoptosis on epithelial barrier function.
Main Methods:
- Utilized camptothecin to induce apoptosis in HT-29/B6 cell monolayers.
- Measured transepithelial electrical resistance (TER) and paracellular permeability using [3H]mannitol flux.
- Assessed single-cell apoptosis conductance via conductance scanning technique.
- Employed Ussing chamber technique for barrier function analysis.
Main Results:
- Camptothecin significantly decreased transepithelial resistance, indicating barrier disruption.
- Increased fluxes of the paracellular marker [3H]mannitol were observed.
- Camptothecin elevated the apoptotic rate and single-cell apoptosis conductance.
- Demonstrated significant epithelial barrier defects in response to camptothecin-induced apoptosis.
Conclusions:
- Camptothecin is a potent inducer of apoptosis in HT-29/B6 cells, causing notable intestinal barrier defects.
- The study provides a foundation for investigating other cytokines, such as TGF-beta, in apoptotic conditions affecting the intestinal barrier.