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Inflammation may cause preterm labor and fetal deaths

was used as the model organism for the study. Around day 16 of the gestation period for the mice (the equivalent of the third trimester for humans), F. nucleatum was injected into three groups of miceone that had TLR4 receptors, a group of TLR4-deficient mice and a group that had TLR4 receptors but were given a synthetic compound to block the receptors inflammatory response. Within eighteen hours, inflammation was present in the TLR4 mice.

The researchers wrote, F. nucleatum colonization in the mouse placenta was accompanied by inflammation, similar to intrauterine infection in humans, suggesting placental inflammatory response as an important factor in the pathogenesis of bacterial-inducted preterm birth.

The researchers found that the TLR4-deficient mice gave birth to healthy pups. The TLR4 group that was not given the synthetic compound to block TLR4 from reacting to bacteria had a 50% increase in fetal death over the mice that had TLR4 but were given the compound to block the inflammatory response. In the TLR4-deficient mice, there were very few fetal deaths.

Han said the synthetic TLR4 antagonist appears to be safe for mice mothers and their pups.

The researchers said they hope to find ways to prevent preterm labor that complicates 12% of all live deliveries and results in 70% of neonatal deaths. Preterm births affect nearly half a million babies in the U.S. each year and cost billions of dollars in health costs annually. Han added that the 30% increase in preterm births in recent decades makes it especially important to investigate novel ways of reversing this trend.


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Contact: Susan Griffith
susan.griffith@case.edu
216-368-1004
Case Western Reserve University
8-Aug-2007


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