A basic communication breakdown may be the culprit behind slower-healing wounds among older individuals, suggests a new study appearing in the journal Cell.
Seeking the answer to a riddle that has long vexed the medical community, a group of scientists from The Rockefeller University in New York asked themselves a simple question: Why do older bodies take longer to heal than their younger counterparts?
What they found hinges on the intricate processes of how – and how quickly – body cells communicate with one another.
“Within days of an injury, skin cells migrate in and close the wound, a process that requires coordination with nearby immune cells. Our experiments have shown that, with aging, disruptions to communication between skin cells and their immune cells slow down this step,” said Elaine Fuchs, head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology at The Rockefeller University in New York.
“This discovery suggests new approaches to developing treatments that could speed healing among older people,” added Fuchs.
The scientists’ study focused on the healing process in mice, but they noted that the human body operates on a similar premise.
Why the Healing Process Is So Complex
“Wound healing is one of the most complex processes to occur in the human body,” noted Brice Keyes, researcher at Calico Life Sciences and co-author of the study. “Numerous types of cells, molecular pathways, and signaling systems go to work over timescales that vary from seconds to months. Changes related to aging have been observed in every step of this process.”
The healing process requires the work of both skin cells and immune cells, which essentially must coordinate with one another to heal a wound effectively. The first visible sign of healing is the formation of a scab, but the healing process continues with a coordinated attack that’s not apparent to the naked eye. After a scab forms, new skin cells called keratinocytes form underneath to repair the damaged skin and sub-skin layers.
For their study, the scientists assessed how quickly keratinocytes traveled in two groups of mice – one group was two months old and the other was 24 months old. Among humans, that’s equivalent to about 20 years old and 70 years old, respectively.
The study authors discovered that keratinocytes traveled far slower in the population of older mice. Specifically, among older mice the keratinocytes failed to release proteins that, when functioning normally, instruct immune cells to help in the healing process, the authors found.
In young mice, the keratinocytes released an abundant amount of proteins that told the immune cells to help out.
When the researchers intervened in the communication process by adding outside protein to the mouse cells, the immune cells in older mice reacted in the same way as the cells of the young mice – “in effect, the old keratinocytes behaved more youthfully,” describes the study.
“Our work suggests it may be possible to develop drugs to activate pathways that help aging skin cells to communicate better with their immune cell neighbors, and so boost the signals that normally decline with age,” Fuchs concluded.