ArticleCell death & disease2019
Elevated apoptosis impairs epithelial cell turnover and shortens villi in TNF-driven intestinal inflammation.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 100 citations in OpenAlex.
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- Positional BMP signaling orchestrates villus length in the small intestine.Nature communications · 2025Article
- miR-369-3p Ameliorates Inflammation and Apoptosis in Intestinal Epithelial Cells via the MEK/ERK Signaling Pathway.International journal of molecular sciences · 2025Article
- Barrier-Strengthening Effects of Cannabidiol on Porcine Peyer's Patches.International journal of molecular sciences · 2025Article
- Bioinformatics-driven insights: rapamycin-mediated CaMK2D inhibition alleviates intestinal ischemia-reperfusion injury.Frontiers in immunology · 2025Article
- Intestinal mucosal turnover in germ-free piglets infected with E. coli.Journal of molecular histology · 2024Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
The intestinal epithelial monolayer, at the boundary between microbes and the host immune system, plays an important role in the development of inflammatory bowel disease (IBD), particularly as a target and producer of pro-inflammatory TNF. Chronic overexpression of TNF leads to IBD-like pathology over time, but the mechanisms driving early pathogenesis events are not clear. We studied the epithelial response to inflammation by combining mathematical models with in vivo experimental models resembling acute and chronic TNF-mediated injury. We found significant villus atrophy with increased epithelial cell death along the crypt-villus axis, most dramatically at the villus tips, in both acute and chronic inflammation. In the acute model, we observed overexpression of TNF receptor I in the villus tip rapidly after TNF injection and concurrent with elevated levels of intracellular TNF and rapid shedding at the tip. In the chronic model, sustained villus atrophy was accompanied by a reduction in absolute epithelial cell turnover. Mathematical modelling demonstrated that increased cell apoptosis on the villus body explains the reduction in epithelial cell turnover along the crypt-villus axis observed in chronic inflammation. Cell destruction in the villus was not accompanied by changes in proliferative cell number or division rate within the crypt. Epithelial morphology and immunological changes in the chronic setting suggest a repair response to cell damage although the villus length is not recovered. A better understanding of how this state is further destabilised and results in clinical pathology resembling IBD will help identify suitable pathways for therapeutic intervention.
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