28 January 2016 Intestine has larger rescue brigade than previously thought Back to news Researchers at the Hubrecht Institute have found that the intestine has a larger regenerative capacity than previously thought. The precursors of the enterocytes, the cells that populate the vast majority of the intestine, are able to return to the stem cell stage. This discovery offers a starting point for further research into the plasticity and regeneration of the intestine, which is of importance in the case of damage as a result of disease. The research is published in Cell Stem Cell this week. The lining of the human intestine renews itself continuously and at high speed. This way, the intestine protects itself against inflammatory processes and chemical and biological influences of enzymes and bacteria. The renewal of the intestine is done by stem cells, which are present in the so-called crypts of the intestine. The newly formed cells leave the crypt and populate the intestinal villi as specialized cells. Research now shows that when the stem cells in the crypt are damaged and no longer function, the precursors of enterocytes can take over this stem cell functionality. Previous research has already shown that the precursors of the secretory cells are able to return to the stem cell stage. However, these secretory cells occupy only a small percentage of the total population of intestinal cells. Paul Tetteh, researcher in the lab of Hans Clevers, has now shown that the precursor of the most present food-processing cell, the enterocyte, also has this possibility. While developing into a specialized cell, the precursor enterocyte can ‘return to base’ to correct the imbalance in stem cells. The intestine has a large reservoir of cells that have the potential to take over stem cell function. This shows that the plasticity of the intestine is much larger than previously thought. This could be of interest for further research into regeneration of the intestine with regard to for example (chronic) inflammatory diseases such as Chron’s disease.