How intestine repairs itself

Researchers at Baylor College of Medicine, Johns Hopkins University School of Medicine and the University of California, San Francisco have gained new insights into how the small intestine, one of the fastest renewing tissues in the human body, repairs itself after injury caused by intestinal rotavirus infection. Their findings have led them to propose that, contrary to the current thinking, how the intestine repairs itself seems to depend on the type of damage, and they found that triggers that were previously thought to be unimportant are actually essential for repairing virus-caused injury.

They studied different damage model, damage caused by rotavirus, a common small intestinal viral infection that affects young children. Repair and turnover of the epithelium, the most external cellular layer of the small intestine responsible for absorption of nutrients and other functions, depend on the intestinal stem cells, regardless of the cause of the damage. There are two types of intestinal stem cells: CBCs (crypt-based columnar cells) and reserve intestinal stem cells. The type of injuries studied until now damages the highly proliferative CBCs, and when these stem cells are destroyed, the reserve intestinal stem cells respond to restore the damage. The response to injury caused by rotavirus, however, is different.

Rotavirus is an infection and has a very specific damage pattern, the virus specifically infects epithelial cells, but not the stem cells. The first finding refers to the type of stem cell involved in the repair of the epithelial cells damaged by the virus. Previous studies had shown that when CBC stem cells are damaged, the reserve stem cells come to their rescue leading the reconstitution of the damaged epithelium. When rotavirus damages the epithelium, but not the stem cells,  the CBCs, not the reserve stem cells, are the primary cell type involved in the restoration of the intestinal epithelium.

 CBCs were not considered important for the repair of intestinal epithelium, but the results show that they are crucial for injury repair after rotavirus-induced epithelial cell damage in contrast to previous studies supporting the reserve intestinal stem cells as the cell type involved in epithelial restitution. The second finding refers to the source of the signaling molecules-called WNTs that trigger the growth and activation of stem cells leading to injury repair. Scientists have described two sources of WNT molecules, epithelial cells and mesenchymal cells. Epithelial WNT molecules were essential to signal the stem cells to repair the damage caused by rotavirus infection.
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