New York: Researchers have found that the immune system may play a role in preventing premature labour and birth.
It was previously known that cytokines — small proteins that alert the body to infection and cause inflammation — are found in the amniotic fluid of many women who gave birth prematurely.
Although the immune system ought to attack the foetus, a foreign body in the mother’s womb, something blocks that from happening during pregnancy.
It means that the protection is stopped for some women, causing premature labour, the researchers said.
“There’s a lot of anti-inflammatory mechanisms that prevent the foetus from being rejected. So we thought maybe dangerous inflammation, that can break down the tolerance barrier, could mediate the start-up of birth even — or especially — premature birth,” said Anthony Vella, an immunologist at the University of Connecticut.
In the study, published in the journal Reproductive Sciences, the team took cells from the female reproductive tract and the amniotic fluid that surrounds foetuses in the womb, and exposed them to pieces of bacteria in the lab.
As expected, the cells produced lots of cytokines, but these were not primarily the inflammation causing ones.
Instead, they saw much more granulocyte-macrophage colony-stimulating factor (GM-CSF) than they expected.
GM-CSF is a kind of cytokine that causes cells to grow up quickly and become bacteria-eating macrophages. The population of macrophages in pregnant women does tend to ramp up right before the women gives birth. It is, however, unclear if that is directly connected to birth, or a side effect of another process.
The finding that GM-CSF is released in response to perceived bacterial infection is intriguing because there’s already a drug available that blocks GM-CSF.
Treating pregnant mice with this drug sharply reduced pre-term birth in mice that had been exposed to pieces of dangerous bacteria. If preventing premature births could be that straightforward, it would be a game changer, the researchers noted.
“We’re hoping to do more immune mechanism studies in mice. And in the not-too-distant future, we hope to start looking at human studies,” the researchers noted.
IANS