Crites, K. S.-M. et al. CFTR Knockdown induces proinflammatory changes in intestinal epithelial cells.
Here, we first uncover changes in intestinal architecture, cell number, and cell composition upon aging.
Synnestvedt K, Furuta GT, Comerford KM et al. Ecto-5'-nucleotidase (CD73) regulation by hypoxia-inducible factor-1 mediates permeability changes in intestinal epithelia.
Hill, D.A. et al. Metagenomic analyses reveal antibiotic-induced temporal and spatial changes in intestinal microbiota with associated alterations in immune cell homeostasis.
No changes in intestinal architecture, cell differentiation, or lineage selection were observed with expression of the transgene.
We further found that the feeding of meat preparations with added nitrate to rats resulted in hyperactivity reminiscent of human mania, alterations in brain pathways that have been implicated in human bipolar disorder, and changes in intestinal microbiota.
Protective type 2 responses against intestinal helminths have been associated with epithelial remodeling mediated by IL-13 and both quantitative and qualitative changes in intestinal mucus, among other mechanisms35,43,44.
Neu J, Reverte CM, Mackey AD, Liboni K, Tuhacek-Tenace LM, Hatch M et al. Changes in intestinal morphology and permeability in the biobreeding rat before the onset of type 1 diabetes.
In conclusion, neither the ectopic expression of Cdx1 was associated with changes in intestinal cell proliferation or differentiation nor was there increased intestinal cancer susceptibility.
In summary, progressive FR increased circulating markers of inflammation, which we speculate is due to increased intestinal permeability as demonstrated by changes in intestinal architecture.
This chapter summarizes the ISC microenvironment in both cells and ECM contexts with the focus on the role of ECM compositional changes in intestinal homeostasis.
