It’s a tale of mice and mankind, of birth and breath and it could eventually lead to important research on breathing disorders including sudden infant death syndrome.
The story is of infant lungs yet to be used suddenly inflating and changing pressure in the heart to alter blood circulation and stimulate the closing of holes between the left and right atria and pushing the baby, which heretofore lived off its mother, to live on its own.
And it all begins with a breath.
University of Virginia researchers, working with mice as well as colleagues at Canada’s University of Alberta and at Harvard University, may have found the key to boot up the baby’s lungs.
In fact, the tiny peptide, a compound containing two or more amino acids joined by peptide bonds, may be involved in keeping the lungs working well long after birth.
“We’ve been long interested in the brain cells that control breathing and one of the main systems are sensor cells that detect carbon dioxide in the body and signal to the brain that we need to breathe more. It’s like a feedback circuit,” said Douglas A. Bayliss, UVa professor of pharmacology and pharmacology chairman.
“We found the cells that do that some years ago, but when we were looking to categorize them, we found the peptide,” he said.
With help from laboratory mice, the researchers found something else. They found a gene that switches on the peptide at just the right time.
“The thing that was incredible to us is that expression of that peptide turns on right at the time of birth,” Bayliss said. “This is an important aspect of how the baby transitions from not having to breathe at all to breathing entirely on its own. It’s pretty amazing.”
Like many scientific revelations, rather than being an answer, the peptide poses more problems.
“There’s a burst of peptide at birth and then a reduction afterward and it makes you wonder, how does the body know to create the peptide? What’s the signal that increases the expression of that peptide? How does it know to reduce production?” Bayliss said.
“It could be like a car engine adjusting to temperature or a sensor,” he said. “Is it the change in body temperature? Is it a change in oxygen levels? We don’t know, yet.”
The peptide could be the lead researchers need in studying breathing difficulties in infants.
“It has this burst [of peptide] and then it tapers off. If you had a disruption in the peptide burst, or if the respiratory system isn’t fully ready to take over as the production tapers off, maybe that leads to problems we’ve seen in infants.”
Researchers discovered that suppressing the peptide production resulted in breathing difficulties and an increase in apneas, which are potentially dangerous pauses in breathing. These apneas further increased with changes in environmental temperature.
These observations suggest that problems with the neuropeptide system might contribute to sudden infant death syndrome, known as SIDS. Might, however, is the key word because the syndrome is still a mystery.
SIDS is a term used to explain the inexplicable death of a healthy baby less than a year old, usually during sleep.
“SIDS is a complicated diagnosis about which we don’t know very much. A lot of times it’s diagnosed by the process of elimination. It wasn’t this or this or this or that, it was SIDS,” Bayliss said. “The brain cells we’re talking about haven’t been well defined in the human brain so whether the peptides result in apneas in humans we can’t say for sure. This gives us something to look for, to see if it may be part of the disorder.”
Next up for the researchers is getting to know more about the peptide in mice.
“We’re interested in learning how the peptide gets turned on, the fundamental biology of it and, with all the things a baby has to take care of at birth, are there other systems creating peptides? Is this a more general phenomenon or specific to breathing? Bayliss said. “The intermediate step is to find out how these changes come about in the system and can we make a link with humans and what we’re finding in mice?”