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Pregnancy
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my personal edition > pregnancy > news
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Researchers Identify Maternal, Fetal Genes That Increase Preterm Birth Risk
BETHESDA, Md -- February 4, 2010 -- Researchers have identified DNA variants in mothers and fetuses that appear to increase the risk for preterm labour and delivery. The DNA variants were in genes involved in the regulation of inflammation and of the extracellular matrix.
The findings, presented today at the Society for Maternal-Fetal Medicine's (SMFM) annual meeting by Roberto Romero, MD, Perinatology Research Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Bethesda, Maryland, may one day lead to new strategies to identify those at risk for preterm birth, and to ways to reduce the occurrence of preterm birth among those at risk.
Dr. Romero described pregnancy as a unique state in which 2 genetically distinct organisms -- mother and fetus -- must coexist. Each fights infection by using hormones that stimulate the immune system. Hormones which play a role in immunity also play a role in labour. When released by either the mother, or the fetus, these hormones set in motion a cascade of events that can cause labour to begin.
"Our hypothesis is that the mother and/or the fetus signal the onset of preterm labour when the environment inside the uterus is unfavourable and threatens the survival of the maternal-fetal pair," said Dr. Romero.
Similar to sensitivity to allergens, the intensity of the immune response varies greatly, depending on genetic factors, the researchers theorised. Presumably, this genetic variability in the immune response accounts for why some pregnancies progress to full term, while others end early.
"When there is an infection in the uterus, the onset of premature labour appears to have survival value," said Dr. Romero. "In the presence of infection, premature labour would allow the mother to rid herself of the infected tissue and preserve her ability to have future pregnancies. If premature labour occurs too early, babies may not survive." If premature labour due to infection occurs late in pregnancy, it may be life-saving for both mother and fetus.
Along with genes controlling the inflammatory response, the researchers also found that DNA variants in genes active in the extracellular matrix were also linked to premature labour. The maternal and fetal genes that Dr. Romero and colleagues identified regulate the amount of extracellular matrix in the uterus. The extracellular matrix of the uterine cervix and of the membranes containing the embryonic fluid are broken down at the beginning of labor.
To conduct the study, they evaluated 190 genes and more than 700 DNA variants in samples from 229 women and 179 premature infants, and a large number of women who delivered at term. The study was conducted on a population of women in Chile. All of the women in the study were of Hispanic origin (of largely white and Native American backgrounds.). The study is one of the few to look at the genetic factors governing birth in an exclusively Hispanic population.
Infants who carried the DNA variant in the gene for the Interleukin 6 receptor were more likely to be born premature than those who did not. In previous studies, Dr. Romero and colleagues found that high levels of Interleukin 6 in the amniotic fluid and in the fetal blood are associated with the beginning of premature labour.
SOURCE: National Institutes of Health
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