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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Inflammation heals skin faster

Wounds and harmful inflammation provoking experiences impart long lasting memories to stem cells in the skin, teaching them to heal subsequent injuries faster. These stem cells, which replenish the skin's outer layer take their cue from the body's response to injury or infection.

The first bout of inflammation sensitizes these cells: the next time they sense it coming, they respond more rapidly. Skin can form memories of an inflammatory response, enhancing responsiveness to inflammation, these memories help the skin maintain its integrity, a feature that is beneficial in healing wounds after an injury.

Whether burned by the sun, attacked by microbes, nicked by a cut, the skin quickly becomes inflamed, swollen, and painful as the body seeks to stop the damage and initiate repair. The immune system maintains a memory of inflammation to mount faster responses to recurrent infections.

 Skin is the body's protective barrier, most of the cells in the skin's outermost layer, the epithelium, don't stick around long enough to form such memories but they migrate up through the epithelium and eventually slough off. Deeper within the epithelium, however, reside the stem cells that are responsible for continually replenishing it. These stem cells remain in place long after the skin has recovered from inflammation; and this experience changes the skin.

In experiments with mice, researchers showed that wounds closed more than twice as fast in skin that had already experienced inflammation than in skin that had never been damaged even if the initial inflammatory experience had occurred as long as six months earlier, inflammation-experienced stem cells were better at moving into the wound to repair the breach.

Inflammation triggers a process that physically opens up distinct sites within the cell's chromosomes, making certain genes accessible for activation. Some of these sites remain open long after the skin has recovered, allowing the genes to be turned on faster during a second round of inflammation.

A gene called Aim2, which encodes damage-and-danger sensing protein, appeared particularly crucial: an initial bout of inflammation prompts a sustained increase in its expression. A second assault quickly activates the protein, resulting in the production of an inflammatory signal that boosts the stem cells' ability to migrate into the wound.
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