Premature births have been entirely prevented in mice with the use of a drug that switches off inflammatory pathways, according to Adelaide researchers, looking to solve the problem in pregnant women.
The team from the University of Adelaide’s Robinson Institute, has been studying the inflammatory mechanisms that lead to pre-term births and how they can be suppressed.
They used plus-naloxone, a drug known to switch off pro-inflammatory pathways, and found they were able to entirely prevent premature birth in pregnant mice.
They also saw infant fatalities were significantly reduced, and the low birth-weight normally associated with pre-term birth was also reversed.
“The babies born to mothers treated with plus-naloxone developed normally and were mostly indistinguishable from those born to the control group,” lead author and Institute director Professor Sarah Robertson said.
The researchers described the results as showing “early promise”.
“Not only did we prevent them being born too soon, we prevented stillbirth and the foetal growth restriction that would otherwise have occurred,” Professor Robertson said.
“[It’s] unusual to find a single molecule in biology that has such a potent effect.”
They said the main causes of premature birth in humans — including bacterial infection, physical injury, placental damage, carrying twins or triplets, or environmental toxins — cause an “inflammatory cascade”.
They said that can activate an immune response in women who will then be unable to carry the baby beyond 37 weeks of pregnancy.