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Increased small bowel epithelial turnover in interleukin-1 receptor knockout mice
S E Wolf1, M A Debroy, H Ikeda
1Department of Surgery, The University of Texas Medical Branch and The Shriners Hospitals for Children, Galveston, Texas, USA. swolf@sbi.utmb.edu
Annals of Surgery
|June 22, 2000
Summary
Mice lacking the interleukin-1 (IL-1) receptor showed increased gut epithelial cell apoptosis and proliferation, indicating faster cell turnover. This study explores gut epithelial homeostasis and turnover mechanisms in vivo.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Gut mucosal integrity relies on balancing cell proliferation and apoptosis.
- Interleukin-1 (IL-1), a pro-inflammatory cytokine, may enhance epithelial cell death via apoptosis.
Purpose of the Study:
- To investigate the effect of interleukin-1 (IL-1) on small bowel mucosal cellular homeostasis.
- To compare apoptosis and proliferation rates in the small bowel epithelium of IL-1 receptor knockout mice versus wild-type controls.
Main Methods:
- Utilized C57BL6 mice, including IL-1 receptor (type I) knockout and wild-type controls.
- Assessed apoptosis using TUNEL staining and proliferation via proliferation cell nuclear antigen (PCNA) staining.
- Analyzed nuclear factor-kappaB (NF-κB) expression in mucosal protein extracts.
Main Results:
- IL-1 receptor null mice exhibited increased percentages of apoptotic and proliferating cells in the small bowel epithelium.
- Despite increased cell turnover, mucosal morphology and the small bowel length to body weight ratio remained unchanged.
- Absence of IL-1 receptors correlated with reduced NF-κB expression.
Conclusions:
- Increased apoptosis and proliferation in gut epithelial cells lacking IL-1 receptors suggest enhanced cell turnover without altering the net balance.
- This mouse model offers a platform for studying in vivo gut epithelial turnover under normal and pathological conditions (proliferation and atrophy).